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Evolution?

stevevw

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Most complex organisms have populations that are plenty big enough for natural selection to be quite effective.
It seems that there are tests that are showing that this is not the case. The problem I have with the MS is that any mutational change is a change to an existing setup that is already finly tuned and working well. The more changes to this the more potential problems regardless of what type of mutation it is. For every beneficial mutational change, there has to be another 99% of neutral and harmful mutations, though there seems to be evidence that the neutral ones are actually well tolerated slightly deleterious mutations anyway.

The point is to account for the high level of variety and complexity that has ever been and what is around today this would require an awful lot of change to what was already good and therefore it seems like taking 5 big steps backwards to get one tiny step forward. It does not make sense. It is not the individual mutation that causes the problem but the accumulation of many mutational changes (epistasis) that is the problem.

These findings, supported by FoldX stability computations of the mutational effects, prompt a new model in which the mutational robustness (or neutrality) observed in proteins, and other biological systems, is due primarily to a stability margin, or threshold, that buffers the deleterious physico-chemical effects of mutations on fitness. Threshold robustness is inherently epistatic-once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed.
Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein. - PubMed - NCBI

Hence there have to be other explanations for how creatures gain that level of complexity other than a process that is blind and random which runs a high chance of introducing harm let along fitter and more complex life. From my research, this seems to be the case such as with ideas like the extended synthesis for one.

No maybe about it: natural selection is highly effective at eliminating deleterious mutations. There is a range of very mildly deleterious and very mildly beneficial mutations that natural selection doesn't effect in species with smallish populations, but they've long since reached equilibrium.
That maybe the case but it seems there are a number of situations where this does not happen. As mentioned above there needs to be an awful lot of mutations happening just to get enough beneficial ones to account for the level of complex life we have. Having so many mutations period is not a good thing. I dont think we know enough about what all these mutational effects are doing. A recent paper mentioned that they are finding more harmful mutations hidden in the genome of humans.

Sometimes selection can even allow not so good mutations to hang around, sometimes selection is overpowered and other times the mutational change is not strong enough to be selected for in the first place. If selection is so good at eliminating these harmful mutations, then why are humans accumulating so many disorders and diseases?

Stability effects of mutations and protein evolvability.
The past several years has seen novel insights at the interface of protein biophysics and evolution. The accepted paradigm that proteins can tolerate nearly any amino acid substitution
has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability—the ability of proteins to acquire changes in sequence and function.
Stability effects of mutations and protein evolvability. - PubMed - NCBI

What threshold? What fitness cost?
Tests done have shown proteins can tolerate a certain amount of slightly deleterious mutations but there is a point where the accumulation of these mutations will begin to affect their fitness. As with the paper below showing that the mutation rate must stay below 6 per genome per generation to avoid the accumulation of too many harmful effects. If natural selection was so efficient at eliminating these mutations, then why are these mutations able to get to the point of affecting the fitness levels of proteins in the first place. Why has 99% of all species especially complex organisms gone extinct?

Beyond A 'Speed Limit' On Mutations, Species Risk Extinction
Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material.
Beyond A 'Speed Limit' On Mutations, Species Risk Extinction

The way I am understanding the below papers is that even beneficial mutations can have harmful effects when pooled with other mutations through epistasis.

Diminishing Returns Epistasis Among Beneficial Mutations Decelerates Adaptation

These results provide the first evidence that patterns of epistasis may differ for within- and between-gene interactions during adaptation and that diminishing returns epistasis contributes to the consistent observation of decelerating fitness gains during adaptation.
Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population
We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations-the larger the expected benefit, the more negative the epistatic effect.

I'm aware of no non-adaptive mechanisms for adaptation, and am unclear on what that might even mean.
There are other processes such as in development, through plasticity, that allows creatures to make well integrated and suited changes that allow them to adapt rather than rely on random mutations that introduce harmful effects that then need to be selected out just to find some beneficial mutational change. This seems like having to go through a risk of harm just to gain some benefit. It seems to me living things do not have to put themselves at risk like this when they have existing inbuilt mechanisms that allow them to tap into genetic info through developmental programs that allow them to adapt.
 
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The Barbarian

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Barbarian observes:
Most complex organisms have populations that are plenty big enough for natural selection to be quite effective.

It seems that there are tests that are showing that this is not the case.

It's what we observe in nature. Darwin's theory predicted that natural selection would increase fitness in a population. The work of Rosemary and Peter Grant in the Galapagos showed just how efficient and how quick that works, even in the rather small populations of finches on Daphne Major. It's just what we observe to happen.

The problem I have with the MS is that any mutational change is a change to an existing setup that is already finly tuned and working well.

It's why we don't see much change in allele frequencies in well-fitted populations. That's what Darwin predicted, and it's what we see. It's why Hardy-Weinberg equilibria are so useful in assessing selective pressures.

The more changes to this the more potential problems regardless of what type of mutation it is. For every beneficial mutational change, there has to be another 99% of neutral and harmful mutations, though there seems to be evidence that the neutral ones are actually well tolerated slightly deleterious mutations anyway.

Since we all have dozens of harmful recessives, that's demonstrably true. But as the record shows, evolution tends to move more quickly in cases of small populations in area where they are not very fit on arrival. That happens all the time, and surely most of the populations die out. But some don't. And there's how it happens. The hawthorne apple fly is a native to America. It has a life cycle closely attuned to the hawthorn fruit on which the larvae live.

Then, Europeans brought apple trees to America. After a while some of the flies began to live on apples. It was a chancy thing, since apples fruit at different times. But eventually there became a population of flies that were adapted to apples. Because their developmental timing was different, they became reproductively isolated from the original population. But somehow, they made it. Now they are an incipient species. That's how it works, much of the time.

The point is to account for the high level of variety and complexity that has ever been and what is around today this would require an awful lot of change to what was already good and therefore it seems like taking 5 big steps backwards to get one tiny step forward.

See above. A year or so to make significant changes in the phenotype of finches in the Galapagos. Maybe 200 years to get a new species of insect. What would that mean if you had a few billion years?

Yep.

It is not the individual mutation that causes the problem but the accumulation of many mutational changes (epistasis) that is the problem.

Most epistatic effects are harmful. Most are neutral. And a few are useful. Without natural selection, it would be a problem.

These findings, supported by FoldX stability computations of the mutational effects, prompt a new model in which the mutational robustness (or neutrality) observed in proteins, and other biological systems, is due primarily to a stability margin, or threshold, that buffers the deleterious physico-chemical effects of mutations on fitness. Threshold robustness is inherently epistatic-once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed.
Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein. - PubMed - NCBI



Hence there have to be other explanations for how creatures gain that level of complexity other than a process that is blind and random

It's called "natural selection." As the Grants showed, the combination of alleles that made finches most fit for their environment, always won out. That's pretty hard to explain in any other way than natural selection.

which runs a high chance of introducing harm let along fitter and more complex life. From my research, this seems to be the case such as with ideas like the extended synthesis for one.

That maybe the case but it seems there are a number of situations where this does not happen. As mentioned above there needs to be an awful lot of mutations happening just to get enough beneficial ones to account for the level of complex life we have.

Let's take a look at that. Humans each have a dozen or so mutations that didn't exist in either of their parents. Suppose there are only a million humans. That mean at least 12 million mutations in a generation. At 25 years to a generation, that means 48 million in a century, or 480 trillion in a million years. Now, humans are a little over 95% gentically identical to chimps. And we have 30,000 genes or so. Which means a 1500 gene difference.

We diverged from chimps a little over 3 million years ago. So that means 1,440,000,000,000 mutations ago. So if the ratio of useful to harmful or neutral mutations was at least 0.0000000001, then it would be fine at the observed mutation rate. Given existing observations of mutations, that's a pretty safe bet.

As mentioned above there needs to be an awful lot of mutations happening just to get enough beneficial ones to account for the level of complex life we have.

Yep. God thought of that.

Having so many mutations period is not a good thing.

The observed rate seems to be working O.K.

I dont think we know enough about what all these mutational effects are doing.

We've got a lot to learn. However, reality is what we see, even if we don't understand all of it.

Tests done have shown proteins can tolerate a certain amount of slightly deleterious mutations but there is a point where the accumulation of these mutations will begin to affect their fitness. As with the paper below showing that the mutation rate must stay below 6 per genome per generation to avoid the accumulation of too many harmful effects. If natural selection was so efficient at eliminating these mutations, then why are these mutations able to get to the point of affecting the fitness levels of proteins in the first place. Why has 99% of all species especially complex organisms gone extinct?

Mostly environmental changes. This is what all the numbers fail to account for. Fitness only counts in terms of environment. And mutations that are slightly harmful in one environment will often be useful or even necessary in other evironments. Sickle cell trait, for example. It's disappearing from people of West African ancestry who live where yellow fever doesn't exist, because it's harmful to a significant number of people who have it. And yet, it's maintained where yellow fever exists, because it's a life-safer for a high percentage of people who have it.

Beyond A 'Speed Limit' On Mutations, Species Risk Extinction
Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material.
Beyond A 'Speed Limit' On Mutations, Species Risk Extinction


And yet we have all those mutations. Even identical twins turn out to have genetic differences because of mutations that happened after an egg divided.

And humans seem to be getting more fit, not less fit. As humans moved into different environments in late stone age times, we see all sorts favorable mutations as they adapt to things like cold, high altitudes, and so on.


There are other processes such as in development, through plasticity, that allows creatures to make well integrated and suited changes that allow them to adapt rather than rely on random mutations that introduce harmful effects that then need to be selected out just to find some beneficial mutational change.

We have a number of mutations that allow us to physiologically adjust to different environments, which other animals don't have. But there are limits to how much that can help. We can, for example, make more RBCs if we live at high altitudes, but that has some health and reproductive drawbacks. More efficient are the mutations that (for example Tibetans have evolved) that work without the drawbacks.

This seems like having to go through a risk of harm just to gain some benefit.

Kind of like capitalism, isn't it? It seems like a rough game, but it works.

It seems to me living things do not have to put themselves at risk like this when they have existing inbuilt mechanisms that allow them to tap into genetic info through developmental programs that allow them to adapt.

If that worked, they would. It seems that the mutation rates for most organisms, are optimal for their particular situation, and that can change with selective pressures.

Current Biology
Volume 7, Issue 8, 1 August 1997, Pages R487-R488

Evolution: Setting the mutation rate
PaulSniegowski1

Abstract
A recent study of X-chromosome and autosome genes in mammals suggests that selective trade-offs are important in the long-term evolution of mutation rates; but recent studies with bacteria show that high mutation rates can nonetheless evolve in the short term in clonal populations.
 
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stevevw

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It's what we observe in nature. Darwin's theory predicted that natural selection would increase fitness in a population. The work of Rosemary and Peter Grant in the Galapagos showed just how efficient and how quick that works, even in the rather small populations of finches on Daphne Major. It's just what we observe to happen.
I have no issue with natural selection being able to select certain features that may provide a benefit over time but what I question is how that feature was produced and the role selection played. The assumption that it is natural selection acting on random mutations is what is producing the beneficial features so quickly is being questions more nowadays.

On the one hand, people say in small populations there is a high chance of deleterious mutations and less of a chance of beneficial ones through genetic drift and therefore the chances of fixing a particular trait quickly are very low. Darwinian evolution should take time because it is blind and therefore will produce a lot of non-beneficial features that need to be sifted out before a beneficial one is found. Natural selection is only one of a number of forces that influence the way living things can change. Influences like mutations, recombination and drift are all random and therefore can overpower selection and prolong a trait being fixed unless it has a very strong advantage.

With a small population on an island where there is not a great amount of environment pressure and where variations of beaks are also beneficial in the population, it is hard to see how it is Darwinian evolution that is behind beak changes happening so quickly. It is more likely an influence like genetic plasticity or through developmental evolution where the Finch’s phenotype is influenced by the environment which then can trigger the right sort of change needed through tapping into existing development programs that are able to vary beaks according to the needs of the finch and then selection will come in to consolidate this.

It's why we don't see much change in allele frequencies in well-fitted populations. That's what Darwin predicted, and it's what we see. It's why Hardy-Weinberg equilibria are so useful in assessing selective pressures.
Darwin actually said that we should see a lot of variation through small increments in the fossil records. Among all those tiny increments we should see a lot of misaligned features from random mutations missing the mark and then weeded out through selection.

If you consider the level of variation and complexity in life, Darwinian evolution would have to be working all the time to achieve this. There are a number of influences that make it hard for evolution to have long periods of stasis and one way or the other adaptations are needed according to evolution through new environments, new additions to populations, genetic drift, making it hard to fix a new allele. Ideas like Hardy-Weinberg equilibria and punctuated equilibrium was introduced to address the anomalies in the fossil record that don’t reflect what is expected from evolution.

I find it hard to reconcile that some species that occupy virtually the same environments can have no or little evolution and some do. Yet at the same time can produce great variation within the same environment which does not fit the MS theory. Because it is assumed that life should be continuously changing additional explanations are needed to explain away any anomalies.

What the evidence fits seems to support what we see with ideas like the extended synthesis where living things have an ability to produce well suited and integrated changes quickly through existing development programs and that all life is based on this. For example, development bias dictates that certain body plans will be produced regardless of environmental pressures and therefore is not open to any possibility through random mutations and being directed by blind natural selection. Or that there is a certain amount of phenotypic variation through development plasticity that is not subjust to genetic change through random mutations.

The Origin of Form Was Abrupt Not Gradual
In modern-day organisms, there is significant plasticity. You don't have to go back 600 million years to see that. If you take a plant and put it in different soil or a different environment, it can look entirely different. The fossil evidence tells us there are different kinds of organisms. The fossil evidence doesn't tell us how to get from one organism to another.

The dynamics of tissues, cells and the molecules they produce are capable of making forms that are very different from one another from the very same set of ingredients. So the question of gaps in the fossil record is not simply a matter of time. It's a matter of an explanatory model that recognizes that a morphological phenotype is not a direct read-out of a genotype.
https://archive.archaeology.org/online/interviews/newman.html

Since we all have dozens of harmful received, that's demonstrably true. But as the record shows, evolution tends to move more quickly in cases of small populations in area where they are not very fit on arrival. That happens all the time, and surely most of the populations die out. But some don't. And there's how it happens. The hawthorne apple fly is a native to America. It has a life cycle closely attuned to the hawthorn fruit on which the larvae live.

Then, Europeans brought apple trees to America. After a while some of the flies began to live on apples. It was a chancy thing, since apples fruit at different times. But eventually there became a population of flies that were adapted to apples. Because their developmental timing was different, they became reproductively isolated from the original population. But somehow, they made it. Now they are an incipient species. That's how it works, much of the time.
This is something that can happen through existing development programs in living things where they can tap into and switch on genetic variations according to their new conditions. There is a fair amount of scope (plasticity) in living things that help them adapt to environments. An example is how a plant that is relocated to a new area can change in form according to the conditions of the new area which can influence its phenotype.

Also, insects can have different features that are switched on and off according to seasonal and environmental conditions. All part of the pre-existing capabilities of living organism’s development and phenotype plasticity. Therefore, it is no surprise that creatures are more self-organised and can adapt quickly, and the adaptations are well suited and integrated.

See above. A year or so to make significant changes in the phenotype of finches in the Galapagos. Maybe 200 years to get a new species of insect. What would that mean if you had a few billion years?
All the modern body plans came about fairly quickly in evolutionary terms 500 million years ago. A year seems quick to get a new feature and 200nyears for a new species, in fact too quick for a blind and random process to be the only mechanism for that change. But then I guess it depends on what is classed as a new species.

If you consider the potential shape possibilities that could be produced that would mean throwing in a lot of non-beneficial shapes into the mix and reducing the chances of finding and fixing the most beneficial beak into the population. It makes more sense that there was a little help from the finch’s own developmental process or there is a certain amount of pre-existing plasticity in the beak that was able to produce the right sort of beak fairly quickly and fixing into the population through selection.

Most epistatic effects are harmful. Most are neutral. And a few are useful. Without natural selection, it would be a problem.
Natural selection will not be able to select out deleterious mutations with small effects. Each of those individual small effects will sit there and their combined effect is what can cause the harm. That is why the idea of sifting mutations to find benefits in among nonbeneficial and potentially harmful mutations as the sole mechanism to produce more healthy and complex life does not make sense or really fit what we see. It makes more sense that life has been equipped with its own mechanisms to change and produce when needed through non-adaptive processes and that primarily mutation is a change to what is already good and primarily something that can gradually undermine things.

It's called "natural selection." As the Grants showed, the combination of alleles that made finches most fit for their environment, always won out. That's pretty hard to explain in any other way than natural selection.
Actually I posted that link to show that what is thought of as neutral mutations can be well tolerated mildly deleterious mutations that will have no apparent effect and therefore be viewed as neutral. It is when these accumulate that the cost to fitness occurs. Natural selection is not able to weed these out because they have been allowed to accumulate and each individual small effect cannot be seen by selection. The impact of a mutational change has to be big for selection to work.

So, as we can see primarily what is classed as neutral may be slightly harmful and along with what is classed as deleterious mutations make up the majority of mutations. Therefore, having a process that has to introduce a lot of potential harm that may often go under the radar for selection just to produce some small rare benefit seems illogical and also does not fit the level of variety and complexity we see. To get that level of change for every benefit there would have to have been truckloads of non-beneficial mutations with a lot of harm. Seems like a backwards way of creating all the spectacular life on earth.

Let's take a look at that. Humans each have a dozen or so mutations that didn't exist in either of their parents. Suppose there are only a million humans. That mean at least 12 million mutations in a generation. At 25 years to a generation, that means 48 million in a century or 480 trillion in a million years. Now, humans are a little over 95% gentically identical to chimps. And we have 30,000 genes or so. Which means a 1500 gene difference.

We diverged from chimps a little over 3 million years ago. So that means 1,440,000,000,000 mutations ago. So if the ratio of useful to harmful or neutral mutations was at least 0.0000000001, then it would be fine at the observed mutation rate. Given existing observations of mutations, that's a pretty safe bet.
But here you have assumed the optimum conditions to fix these beneficial mutations are already in place. Where there are not optimum situations there can be an increase in non-beneficial mutations as well. Being that humans transitioning from apes will have had very small populations the chances of there being more conditions that will prevent the right mutations and fixation from influences like drift are much higher.

Studies have shown that there can be a big-time problem for the evolution from ape to human which can stretch out the time to well beyond the 6 million years that evolution claims can happen. This has implications for all small populations for which vertebrates are made up of. But the paper also shows there is still a problem with even larger populations. That is why I think there had some guiding factor that allows life to find the right genetic information within its own makeup to help it adapt.

The waiting time problem in a model hominin population
In a population of 10,000 the establishment of a string of just two specific co-dependent mutations tends to be extremely problematic (conservatively requiring an average waiting time of at least 84 million years). For nucleotide strings of moderate length (eight or above), waiting times will typically exceed the estimated age of the universe – even when using highly favourable settings.
The waiting time problem in a model hominin population

And yet we have all those mutations. Even identical twins turn out to have genetic differences because of mutations that happened after an egg divided.
Yes, there may be certain genetic or even non-genetic alterations that allow variations. These are more to do with developmental plasticity or epigenetics.

And humans seem to be getting more fit, not less fit. As humans moved into different environments in late stone age times, we see all sorts of favourable mutations as they adapt to things like cold, high altitudes, and so on.
Once again this does not make sense in the light of evolution which acknowledges that beneficial mutations are very rare. If in such a short time many favourable mutations happened then neutral and potentially harmful mutations must have happened many times above this as well as beneficial mutations are only a tiny fraction of the total mutations. This speaks more about guided mutations that are a natural part of how life is able to change through self-organised well suited developmental changes that happen through a number of non-adaptive processes as mentioned.

Humans and animals can also adapt to environments by altering their surroundings through niche construction. Rather than having to be adapted to environments they change environments to be more accommodating. In this way, natural selection is relegated to the background as humans are directing what happens.

Kind of like capitalism, isn't it? It seems like a rough game, but it works.
Actually, capitalism, as promoted through neoliberalism, is causing a lot of problems and the system is about to collapse again even worse than with the GFC in 2008. Any system that makes possessions as the most important thing and causes some to have a lot and others to perish through not having enough is doomed to failure.

If that worked, they would. It seems that the mutation rates for most organisms, are optimal for their particular situation, and that can change with selective pressures.
How do you know the changes were the result of random mutations. A form of mutation (a change to existing genetic info) can happen through development processes where a gene is switched on that can produce a new feature to help a creature adapt.

Current Biology
Volume 7, Issue 8, 1 August 1997, Pages R487-R488
Evolution: Setting the mutation rate
PaulSniegowski1
Abstract
A recent study of X-chromosome and autosome genes in mammals suggests that selective trade-offs are important in the long-term evolution of mutation rates; but recent studies with bacteria show that high mutation rates can nonetheless evolve in the short term in clonal populations.
It seems that even though lab tests have shown that there can be an increase in mutations this has been done by introducing an artificially high number of mutator strains which will take over the wild-type bacteria. As a consequence of these experiments, mutated alleles that have been associated with pathogenicity and cancers have resulted. I am sure that under lab conditions all sorts of changes can be mutated after all we have genetic engineering. But it is in the wild where we can see how things really work and it seems that most of the time most mutations are changing what is already working well and are a threat to existing protein structures.
 
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The Barbarian

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Barbarian observes:
It's what we observe in nature. Darwin's theory predicted that natural selection would increase fitness in a population. The work of Rosemary and Peter Grant in the Galapagos showed just how efficient and how quick that works, even in the rather small populations of finches on Daphne Major. It's just what we observe to happen.

I have no issue with natural selection being able to select certain features that may provide a benefit over time but what I question is how that feature was produced and the role selection played.

When we look closely, as the Grants did on Daphne Major, it turns out to work as Darwin said. Drought conditions produced fewer seeds to eat, and those were large with tough husks. Even a millimeter difference in beak length affected survival. And natural selection determined that the next generation would have more robust beaks.

The assumption that it is natural selection acting on random mutations is what is producing the beneficial features so quickly is being questions more nowadays.

Observation, not assumption. It's what the Grants observed to happen.

On the one hand, people say in small populations there is a high chance of deleterious mutations and less of a chance of beneficial ones through genetic drift and therefore the chances of fixing a particular trait quickly are very low.

It's true. This is why speciation isn't more common than it is. Most such populations die out. A few get lucky. But where a favorable trait appears, it will reach fixation much faster in a small population. The startling thing is how fast it can happen. Much faster than Darwin supposed.

Darwinian evolution should take time because it is blind and therefore will produce a lot of non-beneficial features that need to be sifted out before a beneficial one is found.

No. Mutations are blind. Darwin's great discovery was that evolution is directed by natural selection.

Natural selection is only one of a number of forces that influence the way living things can change. Influences like mutations, recombination and drift are all random

And provide the raw material for natural selection. Without mutations (recombination is a mutation, and genetic drift is just evolution in the absence of selective forces on the particular mutation) natural selection could do nothing.

and therefore can overpower selection and prolong a trait being fixed unless it has a very strong advantage.

That's not what was observed. The beauty of the Grants work was that they managed to catalogue all the individuals on the island. So they could precisely determine what was going on.

With a small population on an island where there is not a great amount of environment pressure and where variations of beaks are also beneficial in the population, it is hard to see how it is Darwinian evolution that is behind beak changes happening so quickly.

Yes. It was a profound drought that quickly changed the population. This is why small founder populations in less than ideal locations so often speciate. It was Mayr's observation that unusual species tend to be found in such places that gave Eldridge and Gould their clue about punctuated equilibrium.

It is more likely an influence like genetic plasticity

All genes are plastic. That's what mutation is about.

or through developmental evolution

You mean "evolutionary development?" It's quite clear that HOX genes are open to mutation as well, and this sort of mutation is also open to natural selection. I don't see why this would be different.

where the Finch’s phenotype is influenced by the environment which then can trigger the right sort of change needed through tapping into existing development programs that are able to vary beaks according to the needs of the finch and then selection will come in to consolidate this.

Show us the mechanism for that. It's a bit vague.

Darwin actually said that we should see a lot of variation through small increments in the fossil records.

Where there are huge numbers of fossils for a single species, we see that. But fossilization is ordinarily rare for land animals; very few of them fossilize. However, the huge number of transitional forms in the fossil record does indicate gradual evolution, albeit with different pacing depending on selective forces.

Among all those tiny increments we should see a lot of misaligned features from random mutations missing the mark and then weeded out through selection.

Like the long tails of very early pterosaurs that gave them stable flight, but limited their maneuverability. Like the tiny limbs of some transitional whales that didn't let them walk, but served no purpose in swimming, either. Yes, there's a lot of that.

If you consider the level of variation and complexity in life, Darwinian evolution would have to be working all the time to achieve this.

No. If you have a well-fitted population in a stable environment, natural selection will actually prevent significant evolution.

There are a number of influences that make it hard for evolution to have long periods of stasis and one way or the other adaptations are needed according to evolution through new environments, new additions to populations, genetic drift, making it hard to fix a new allele.

See above. Drift would only occur where there was no significant selective value to any of the alleles involved. As the Grants showed, things stay stable unless there's a change in the environment.

Ideas like Hardy-Weinberg equilibria and punctuated equilibrium was introduced to address the anomalies in the fossil record that don’t reflect what is expected from evolution.

Actually, the Hardy-Weinberg equation is used to determine whether or not there is significant selective pressure. And punctuated equilibrium depends on Darwin's prediction that evolution should not happen if there are no selective pressures to do so. It also fits Huxley's prediction that evolution should go very quickly if the selective pressures are high.

I find it hard to reconcile that some species that occupy virtually the same environments can have no or little evolution and some do.

For example, whales over the past 40 million years have evolved greatly, while sharks in the same environment have evolved very little. It's clear to me why this is so. Does it seem unclear to you?

Yet at the same time can produce great variation within the same environment

Take the case of fruit flies in Hawaii. Few insects managed to get to Hawaii, and so when the ancestral flies got there, they went through an explosion of speciation. Do you see why? It was very predictable in evolutionary theory. On the other hand, the same sort of fly seen in say, Brazil hasn't evolved much during the same period. As Darwin pointed out, this is what you would expect.

Because it is assumed that life should be continuously changing additional explanations are needed to explain away any anomalies.

This doesn't seem anomalous. It's pretty much standard Darwinian evolution.

What the evidence fits seems to support what we see with ideas like the extended synthesis where living things have an ability to produce well suited and integrated changes quickly through existing development programs and that all life is based on this.

For example, eyes evolved numerous times, but most of them depend on the same Hox genes. It seems that opsins were already present in eyeless bilaterans, and those developmental genes for vison existed long before eyes. Since even humans can detect light without eyes, that's not surprising.

For example, development bias dictates that certain body plans will be produced regardless of environmental pressures and therefore is not open to any possibility through random mutations and being directed by blind natural selection.

How does the natural selection that makes organisms more fit for their environment differ from blind natural selection? And what body plans have appeared that prevented any significant changes in them? I can't think of any.

Or that there is a certain amount of phenotypic variation through development plasticity that is not subjust to genetic change through random mutations.

You, for example, can make more red blood cells if you live at a higher altitude. But it isn't passed on to your children.

The Origin of Form Was Abrupt Not Gradual


Let's take us. How long did it take to get from the first chordate to us? What's your estimate?

The fossil evidence doesn't tell us how to get from one organism to another.

It clearly shows how to get from tetrapods to whales. Or from dinosaurs to birds.

The dynamics of tissues, cells and the molecules they produce are capable of making forms that are very different from one another from the very same set of ingredients. So the question of gaps in the fossil record is not simply a matter of time.

Let's test that belief. Tell us of any two major groups, said to be evolutionarily connected, that don't have a transitional form between them.

Also, insects can have different features that are switched on and off according to seasonal and environmental conditions.

And your claim is that such individual variation can't evolve?

All the modern body plans came about fairly quickly in evolutionary terms 500 million years ago.

550 millon years old at least for some of them. 505 million years old for chordates. So perhaps over a period of 45 million years, most of the modern body plans came about. There area few exceptions of phyla that appeared after the cambrian.

A year seems quick to get a new feature

It can happen in one generation.

and 200nyears for a new species

That can happen in one generation also, for organisms that can survive polyploidy.

in fact too quick for a blind and random process to be the only mechanism for that change.

As you learned, natural selection is the antithesis of randomness. So that's really no concern in the real world.

But then I guess it depends on what is classed as a new species.

If you consider the potential shape possibilities that could be produced that would mean throwing in a lot of non-beneficial shapes into the mix and reducing the chances of finding and fixing the most beneficial beak into the population.

As you now see, even a millimeter's difference made a difference in survival long enough reproduce. So it worked very rapidly. Again, in the real world, not in some hypothesis.

It makes more sense that there was a little help from the finch’s own developmental process or there is a certain amount of pre-existing plasticity in the beak

Not in the the beak. In DNA. That is where the "plasticity" lies. Mutations change things. If such a change was inherent in all finches, they would have all changed.

Natural selection will not be able to select out deleterious mutations with small effects.

Until, as happened with the finches, they became significantly deleterous. And then they were removed. That's what you're missing. Fitness only counts in terms of environment.

That is why the idea of sifting mutations to find benefits in among nonbeneficial and potentially harmful mutations as the sole mechanism to produce more healthy and complex life does not make sense or really fit what we see.

Animal and plant breeders do that constantly. And it almost always works.

It makes more sense that life has been equipped with its own mechanisms to change and produce when needed through non-adaptive processes

That is an adaptive process. Mutation and natural selection tend to increase fitness over time in a population. Always have.

Actually I posted that link to show that what is thought of as neutral mutations can be well tolerated mildly deleterious mutations that will have no apparent effect and therefore be viewed as neutral. It is when these accumulate that the cost to fitness occurs.

Which then makes them visible to natural selection, and the inevitable happens.

Natural selection is not able to weed these out because they have been allowed to accumulate and each individual small effect cannot be seen by selection.

But as you now see, as soon as they significantly affect fitness, natural selection removes them.

The impact of a mutational change has to be big for selection to work.

Less than a millimeter's difference in the length of a breastbone in sparrows makes a difference to winter survival in Chicago. So it's rather tiny.

Therefore, having a process that has to introduce a lot of potential harm that may often go under the radar for selection just to produce some small rare benefit seems illogical and also does not fit the level of variety and complexity we see.

And yet it works.

To get that level of change for every benefit there would have to have been truckloads of non-beneficial mutations with a lot of harm. Seems like a backwards way of creating all the spectacular life on earth.

He seems to have done it in the best possible way.

But here you have assumed the optimum conditions to fix these beneficial mutations are already in place.

You're forgetting again. Fitness only counts in terms of the environment.
 
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Barbarian observes:
It's what we observe in nature. Darwin's theory predicted that natural selection would increase fitness in a population. The work of Rosemary and Peter Grant in the Galapagos showed just how efficient and how quick that works, even in the rather small populations of finches on Daphne Major. It's just what we observe to happen.
I am not disputing the mechanism of natural selection. It stands to reason that if robust beaks were needed to get to the seeds then finches with robust beaks would have more of a chance to survive. Natural selection is like a logical equation and can be applied to a lot of things. Only the fittest and most capable athletes will survive through to the finals and the weaker ones will be culled out etc.

But what is observed does not tell us how things happened, and natural selection is only part of what makes evolution work. It is an assumption to think that all change is caused by Neo-Darwinism. Natural selection only tells us about the survival of the fittest and not the arrival of the fittest.

The finch’s developmental program may have been switched on for the component in the gene for a bigger beak rather than random mutations throwing up all sorts of different forms of beaks. So, it was not a random process such as random mutations that produced the variation, but the finch’s developmental program and natural selections role was reduced because the trait was already well suited and integrated.

Evolutionary developmental biology

Among the key empirical insights are that phenotypic variation often involves changes in the gene regulatory machinery that alters the timing, location, amount or type of gene product. This modification of pre-existing developmental processes can bring about coordinated changes in suites of characters, effectively enabling diversification through the differential coupling and decoupling of phenotypic modules [1619]. As a consequence, developmental properties can affect the rates and patterns of phenotypic evolution [20,21] and contribute to evolvability, the potential of biological lineages for adaptive evolution [19,2224].

Of particular interest is the observation that phenotypic variation can be biased by the processes of development, with some forms more probable than others [12,17,2528].


Some work on developmental bias suggests that phenotypic variation can be channelled and directed towards functional types by the processes of development [27,28]. The rationale is that development relies on highly robust ‘core processes’, from microtubule formation and signal transduction pathways to organogenesis, which at the same time exhibit ‘exploratory behaviour’ [28], allowing them to stabilize and select certain states over others.


Exploratory behaviour followed by somatic selection enables core processes to be responsive to changes in genetic and environmental input, while their robustness and conservation maintain their ability to generate functional (i.e. well integrated) outcomes in the face of perturbations. This phenomenon, known as facilitated variation [28,34], provides a mechanistic explanation for how small, genetic changes can sometimes elicit substantial, non-random, well-integrated and apparently adaptive innovations in the phenotype.


Developmental plasticity
There is renewed interest in plasticity as a cause, and not just a consequence, of phenotypic evolution. For example, plasticity facilitates colonization of novel environments [40,41], affects population connectivity and gene flow [42], contributes to temporal and spatial variation in selection [4345] and may increase the chance of adaptive peak shifts, radiations and speciation events [27,4648].

Particularly contentious is the contribution of plasticity to evolution through phenotypic and genetic accommodation [27,48,49]. Phenotypic accommodation refers to the mutual and often functional adjustment of parts of an organism during development that typically does not involve genetic mutation [27].

The extended evolutionary synthesis: its structure, assumptions and predictions

Constructive development
Constructive development refers to the ability of an organism to shape its own developmental trajectory by constantly responding to, and altering, internal and external states [34,71,102105]. Constructive development goes beyond the quantitative-genetic concept of gene–environment interaction by attending to the mechanisms of development and emphasizing how gene (expression) and environment are interdependent.

The extended evolutionary synthesis perspective
Developmental processes play important evolutionary roles as causes of novel, potentially beneficial, phenotypic variants, the differential fitness of those variants, and/or their inheritance (i.e. all three of Lewontin's [98] conditions for evolution by natural selection). Thus, the burden of creativity in evolution (i.e. the generation of adaptation) does not rest on selection alone [12,19,25,27,60,64,73,99101].

The structure of the EES.
Explaining the origin of adaptations requires understanding how pre-existing developmental processes generate heritable phenotypic variants from genetic, epigenetic and environmental inputs.

The EES is thus characterized by the central role of the organism in the evolutionary process, and by the view that the direction of evolution does not depend on selection alone and need not start with mutation. The causal description of an evolutionary change may, for instance, begin with developmental plasticity or niche construction, with genetic change following [27,73]. The resulting network of processes provides a considerably more complex account of evolutionary mechanisms than traditionally recognized (figure 2).

The most striking and contentious difference from the original MS concerns the relative significance of natural selection versus generative variation in evolution, one of the oldest controversies in evolutionary biology (e.g. [116,117]). In the EES, developmental processes, operating through developmental bias, inclusive inheritance and niche construction, share responsibility for the direction and rate of evolution, the origin of character variation and organism–environment complementarity.

Both developmental bias and niche construction impose directionality on evolution, partly because developmental mechanisms have been shaped by prior selection [73], but also because, like other exploratory behaviour within the organism, learning allows organisms to generate and refine novel behavioural variants that are coherent and adaptive [73,118]. Other types of bias may also affect variation and selection, such as systematic biases in mutation [25,116,117,119121], or other historical contingencies, such as learned traditions [66,73].

As a consequence, the EES predicts that organisms will sometimes have the potential to develop well-integrated, functional variants when they encounter new conditions, which contrasts with the traditional assumption of no relationship between adaptive demand and the supply of phenotypic variation [5,122]. For example, phenotypic plasticity and non-genetic inheritance contributed to the adaptation of the house finch to cold climates during its North American range expansion ([68]; see [27,28,49,101,105,107] for further examples).


Other large phenotypic effects occur when developmental processes respond phenotypically to environmental challenges with developmental threshold effects [124], coordinated responses in suites of traits [63] or multiple, stress-induced epigenetic changes [60]. This contrasts with the classical emphasis on gradualism [125,126], which followed from the assumption that, to be adaptive, mutations must have small effects. What the historical rejection of saltationism overlooked was that mechanisms of developmental adjustment allow novel structures to be effectively integrated.

Another distinctive feature of the EES is its recognition that adaptation can arise through both natural selection and internal and external constructive processes. For instance, organisms can respond plastically to novel conditions to generate functional variation. While plasticity is well recognized within the field, what is less well appreciated is that the specific adaptive phenotypes generated need not be the direct targets of past selection, but may be the expression of the more general ability of developmental processes to accommodate novel inputs adaptively, thereby enabling functionally integrated responses to a broad range of conditions [27,34]. Moreover, through niche construction, environments can be changed by organisms to benefit themselves.

This recognition of a variety of distinct routes to phenotype–environment fit furnishes the EES with explanatory resources that traditional perspectives lack. For instance, the well-adapted character of small populations, traditionally regarded as puzzling as selection is weak [128], can potentially be accounted for by the flexible forms of plasticity and niche construction that result from constructive development. In fact, the conceptual change associated with the EES is largely a change in the perceived relationship between genes and development: a shift from a programmed to a constructive view of development.

About the EES - Extended Evolutionary Synthesis

It seems the environment can influence the development of phenotypic shapes through cells and tissues also. So, when a creature is under environmental pressure that pressure may act on the creature’s body which in turn activates the development program to produce the required phenotypic changes. Perhaps just as the finch’s beak is the body part being put under pressure to break open husks this pressure on the beak can activate the development program of the beak to produce bigger beaks i.e. (well suited) change.
 
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sfs

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I don't know what your intentions are, but what you are doing in practice is to spray a bunch of quotes from papers that do nothing to support your claims of problems with evolution by random mutation and natural selection.

For example...
These findings, supported by FoldX stability computations of the mutational effects, prompt a new model in which the mutational robustness (or neutrality) observed in proteins, and other biological systems, is due primarily to a stability margin, or threshold, that buffers the deleterious physico-chemical effects of mutations on fitness. Threshold robustness is inherently epistatic-once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed.
Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein. - PubMed - NCBI
This paper says that each deleterious mutation to a single protein get progressively more deleterious as more of them accumulate. In the real world, however, deleterious mutations are purged by natural selection before any substantial number accumulate in a single protein, so why are you quoting this paper?

And take this one...
Beyond A 'Speed Limit' On Mutations, Species Risk Extinction
Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material.
Beyond A 'Speed Limit' On Mutations, Species Risk Extinction
This paper argues that the maximum supportable mutation rate is 6 nonsynonymous mutations per generation. That's the maximum number of mutations in genes, and counts only those that change the protein. That's roughly 1% of mutations for humans, which means our mutation rate is ten times lower than this limit. So again, why are you quoting this paper?

Where are you getting these papers from? Have you read them? Do you understand the biology in them?
 
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The Barbarian

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But what is observed does not tell us how things happened, and natural selection is only part of what makes evolution work. It is an assumption to think that all change is caused by Neo-Darwinism. Natural selection only tells us about the survival of the fittest and not the arrival of the fittest.

Luria and Debruck showed that was a matter of random mutation, acted upon by natural selection.

It seems the environment can influence the development of phenotypic shapes through cells and tissues also. So, when a creature is under environmental pressure that pressure may act on the creature’s body which in turn activates the development program to produce the required phenotypic changes. Perhaps just as the finch’s beak is the body part being put under pressure to break open husks this pressure on the beak can activate the development program of the beak to produce bigger beaks i.e. (well suited) change.

We know that natural selection does that. But what in the"development program of beak" (assuming there is a "beak program", which is by no means demonstrated) do you think would do that?
 
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Job 33:6

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I don't know what your intentions are, but what you are doing in practice is to spray a bunch of quotes from papers that do nothing to support your claims of problems with evolution by random mutation and natural selection.

For example...

This paper says that each deleterious mutation to a single protein get progressively more deleterious as more of them accumulate. In the real world, however, deleterious mutations are purged by natural selection before any substantial number accumulate in a single protein, so why are you quoting this paper?

And take this one...

This paper argues that the maximum supportable mutation rate is 6 nonsynonymous mutations per generation. That's the maximum number of mutations in genes, and counts only those that change the protein. That's roughly 1% of mutations for humans, which means our mutation rate is ten times lower than this limit. So again, why are you quoting this paper?

Where are you getting these papers from? Have you read them? Do you understand the biology in them?

Just out of curiosity on the last paragraph there, how did you derive that our mutation rate is "10 times lower than this limit"?

Are you saying that in people, we only experience 0.6 non-synonymous mutations per generation?
 
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sfs

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Are you saying that in people, we only experience 0.6 non-synonymous mutations per generation?
Yes, something in that ballpark. We have on average roughly 60 new mutations per generation. Coding sequence for genes represents about 1.5% of the genome, and something like a third of coding mutations are synonymous. So figure about 0.6 nonsynonymous mutations per generation. (For comparison with the model in this paper, the right number is probably half that, the number of nonsynonymous mutations per genome copy.)
 
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Job 33:6

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Yes, something in that ballpark. We have on average roughly 60 new mutations per generation. Coding sequence for genes represents about 1.5% of the genome, and something like a third of coding mutations are synonymous. So figure about 0.6 nonsynonymous mutations per generation. (For comparison with the model in this paper, the right number is probably half that, the number of nonsynonymous mutations per genome copy.)

Ah i see.

Yea that seems strange then that @stevevw would reference such a paper.
 
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stevevw

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I don't know what your intentions are, but what you are doing in practice is to spray a bunch of quotes from papers that do nothing to support your claims of problems with evolution by random mutation and natural selection.

For example...

This paper says that each deleterious mutation to a single protein get progressively more deleterious as more of them accumulate. In the real world, however, deleterious mutations are purged by natural selection before any substantial number accumulate in a single protein, so why are you quoting this paper?

And take this one...

This paper argues that the maximum supportable mutation rate is 6 nonsynonymous mutations per generation. That's the maximum number of mutations in genes, and counts only those that change the protein. That's roughly 1% of mutations for humans, which means our mutation rate is ten times lower than this limit. So again, why are you quoting this paper?

Where are you getting these papers from? Have you read them? Do you understand the biology in them?
The papers come from my database which came from past research into the topics over many years. I have read the papers as I have access to them through my Uni and have used them several times in the past. I am not a biologist so I may not have a complete understanding of their context but I get the basic idea of them. My point is not to deny evolution but to question the source of variations when it comes to random mutations and the prominence of natural selection as being the only process that directs evolution. It seems that though random mutations do provide variation, that variation is often deleterious and harmful. I understand how natural selection can weed out harmful mutations but because many are very slight they are missed and accumulate.

My main disagreement is that a mechanism of random mutations that primarily changes/disrupts what is already good and working well is the best way for how living things can change for the better and become fitter and more complex. Basically, the DNA has repair processes for mutational changes because they are an error and threat to the existing setup. So Neo-Darwinism is banking on basically something that undoes what is good to make something better which does not make sense, especially with Gods creation.

As with the many papers that highlight the fact that random mutations can cause harm Neo-Darwinism not only hinges on natural selection spotting and weeding out all those harmful effects but also highlighting very rare beneficial mutations. It is too risky and God would have installed something that worked better with the existing setup and produced well suited and integrated changes as seen with the processes talked about in the EES and the like.

The paper was not just talking about the individual deleterious mutation but also how the mutations act together and affect each other. Even beneficial mutations can have a negative effect on each other. So it is not just the accumulation of slight mutations but when there is more than one mutation no matter what type of mutation the effect they have with each other can be harmful to fitness.

Also if the mutations are very slight then how can natural selection pick them up in the first place? If natural selection purged these slight mutations before any substantial number accumulate then why do papers state that slight mutations have accumulated to the point of causing harm to fitness? Why do for examples humans have many diseases and disorders from these accumulated mutations. Why has 99% of all complex species gone extinct? Surely some if not a lot of these extinctions were caused by the harmful effects of random mutations on fitness.

My point as from the other papers on alternative sources of variation (EES) is that these sources provide more suitable and stable variation that does not undermine the genome and it makes more sense that this would be a better and logical way that living things can adapt to their environments. As the papers say natural selection and random mutations may have been overstated as the mechanisms and that these other processes are causes and direct evolution.
 
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sfs

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It seems that though random mutations do provide variation
Correct.
that variation is often deleterious and harmful. I understand how natural selection can weed out harmful mutations
Correct.
but because many are very slight they are missed and accumulate.
Incorrect, with a couple of caveats. First, in a very small population of nonrecombining organisms, Muller's ratchet can take over and the accumulation of deleterious mutations rapidly drives the population to extinction. Second, when a population's size decreases, purifying selection becomes somewhat less effective, and mildly deleterious mutations can accumulate until a new equilibrium is reached.
My main disagreement is that a mechanism of random mutations that primarily changes/disrupts what is already good and working well is the best way for how living things can change for the better and become fitter and more complex.
Your disagreement is with reality, then, because random mutations really do make organisms fitter and create new complexity.
As with the many papers that highlight the fact that random mutations can cause harm Neo-Darwinism not only hinges on natural selection spotting and weeding out all those harmful effects but also highlighting very rare beneficial mutations.
Natural selection doesn't have to do any spotting; it just happens. If a mutation is deleterious, then the creature won't reproduce as well and the mutation disappears. It's just statistics.
It is too risky and God would have installed something that worked better with the existing setup
I'm not sure that telling God how he could have done it better is a good plan.
produced well suited and integrated changes as seen with the processes talked about in the EES and the like.
Everything in the EES also ultimately relies on random mutations being filtered by natural selection to produce adaptation.
If the mutations are very slight then how can natural selection pick them up in the first place?
You have to be quantitative -- how slight do you mean? The probability that a beneficial allele with selective advantage s will be picked up is approximately 2s. If that's larger than twice the population size (which is the probability that a neutral mutation will end up fixing by chance), then natural selection has produced a bias towards improvement.
If natural selection purged these slight mutations before any substantial number accumulate then why do papers state that slight mutations have accumulated to the point of causing harm to fitness? Why do for examples humans have many diseases and disorders from these accumulated mutations.
Deleterious mutations continue to be added to the population, and they persist for a while before being purged by purifying selection -- the less deleterious they are, the longer they persist. This equilibrium, between the introduction of new deleterious mutations and the purging of existing ones, is known as mutation-selection balance. It means we all carry a substantial number of deleterious variants that put us as risk for different diseases.
My point as from the other papers on alternative sources of variation (EES) is that these sources provide more suitable and stable variation that does not undermine the genome and it makes more sense that this would be a better and logical way that living things can adapt to their environments. As the papers say natural selection and random mutations may have been overstated as the mechanisms and that these other processes are causes and direct evolution.
I've read just about all of the EES people, and I haven't seen anything proposed as a source of adaptive evolution that doesn't end up relying on random mutation and natural selection.
 
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Job 33:6

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This paper argues that the maximum supportable mutation rate is 6 nonsynonymous mutations per generation. That's the maximum number of mutations in genes, and counts only those that change the protein. That's roughly 1% of mutations for humans, which means our mutation rate is ten times lower than this limit. So again, why are you quoting this paper?

Where are you getting these papers from? Have you read them? Do you understand the biology in them?

@stevevw , I would like to see a specific response to this^.

From what I can gather, you have sourced a paper suggesting that X amount of mutations would lead an organism to ruin. But if mankind were to undergo less of said mutations, then it sounds as though the paper, while interesting, doesn't really hold meaning to the discussion.

For what purpose, did you source this particular paper?

With your words, you said "My point is not to deny evolution but to question the source of variations when it comes to random mutations and the prominence of natural selection as being the only process that directs evolution."

What does this paper do (Beyond A 'Speed Limit' On Mutations, Species Risk Extinction), to serve that purpose?
 
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stevevw

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@stevevw , I would like to see a specific response to this^.

From what I can gather, you have sourced a paper suggesting that X amount of mutations would lead an organism to ruin. But if mankind were to undergo less of said mutations, then it sounds as though the paper, while interesting, doesn't really hold meaning to the discussion.

For what purpose, did you source this particular paper?

With your words, you said "My point is not to deny evolution but to question the source of variations when it comes to random mutations and the prominence of natural selection as being the only process that directs evolution."

What does this paper do (Beyond A 'Speed Limit' On Mutations, Species Risk Extinction), to serve that purpose?
I understood the paper to be saying that living things can only tolerate a certain amount of mutations and therefore risk extinction. I have posted a number of papers along these lines. But it is the accumulation of perhaps small amounts of slightly harmful mutations that are doing the damage. It is not just about extinction but the cost of fitness along the way. Hence the high number of diseases and disorders humans have.

There is a debate about what mutations represent and the level of tolerance populations can handle. I am not saying there is a specific amount of mutations that bring a creature to ruin but that random mutations are basically an error in what is already working good and the fact that the DNA has a mechanism to correct those errors shows that mutations are not meant to be something that can create fitter and more complex life. It seems that evolution wants to find rare exceptions to the rule among something that undermines the genome to create better genomes.

It does not make sense and as I have mentioned that there are other more directed ways that do not have to take this risk and are more directed and designed to allow living things to change as with some of the processes in the EES. There is even evidence of non-random mutations that are triggered through responses to environmental pressures that target specific sections of the genome that enable creatures to adapt. But these are not really mutations in the way Neo-Darwinism understands them but are something that life was designed with as part of their development.
 
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Job 33:6

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Much of the above is vague.

"I understood the paper to be saying that living things can only tolerate a certain amount of mutations and therefore risk extinction. I have posted a number of papers along these lines. But it is the accumulation of perhaps small amounts of slightly harmful mutations that are doing the damage. It is not just about extinction but the cost of fitness along the way. "

Like this statement^. Nothing is actually being said here. The idea that organisms can only tolerate a certain number of mutations is of course a given. And of course the accumulation of small amounts of harmful mutations, will ultimately result in a species going extinct after harming a species before hand.
 
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Job 33:6

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" am not saying there is a specific amount of mutations that bring a creature to ruin"

Nothing said here either.

"random mutations are basically an error in what is already working good and the fact that the DNA has a mechanism to correct those errors shows that mutations are not meant to be something that can create fitter and more complex life. "

Also meaningless. Obviously mutations aren't sentient with a goal of creating a more fit organism. But this doesn't mean that they don't play a role in increasing fitness.

And the fact that the correcting mechanisms for mutations are not full proof, suggests that mutations are meant to be something that can create fitter and more complex life.

See what I did there? Meaningless conjecture.
 
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stevevw

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Nothing said here either.
First off I noticed you did not address what was said about non-random directed mutations being a source of variation rather than random mutations which is the main source of variation for neo Darwinism.

I am not being specific about what level of mutation that causes fitness loss as there is contention about this. The range of mutations being passed on to each generation is said to be from around 60 to 300 mutations. There is a debate about neutral mutations having no effect on fitness as they slightly change existing sequences and therefore take up space which then requires more energy for an organism to accommodate hence a fitness cost. Given enough buildup and they begin to have a cost to fitness. Mutations do not always act in isolation so a slightly harmful change in one nucleotide can also be linked to others throughout the DNA and therefore can hard to eradicate.

As seen with recent research humans are accumulating many slightly harmful mutations and natural selection cannot keep up in purging them out of our genomes so therefore we have a building number of diseases. Beneficial mutations are said to also come with a cost as they also reduce genetic function with any perceived benefit they give. Evidence shows that the more mutations are added the more the cost to fitness regardless of what type of mutation including beneficial mutations through epistasis. So it is not as simple as claiming there are only certain situations where mutations can cause harm and where natural selection can purge out these harmful mutations.

"random mutations are basically an error in what is already working good and the fact that the DNA has a mechanism to correct those errors shows that mutations are not meant to be something that can create a fitter and more complex life. "

Also meaningless. Obviously mutations aren't sentient with a goal of creating a more fit organism. But this doesn't mean that they don't play a role in increasing fitness.
So, it is acknowledged that mutations are an error to what is already fit and working well but somehow some got through and still increase fitness.

Even if we believed that we would need a multitude of beneficial mutations at only 1% of all mutations to get the level of variety and complexity we have today. If that's the case we would also need an overwhelming amount of harmful mutations as well. Under normal circumstances this level of mutations is associated with sickness, malfunction and cancer let along creating something fitter.

And the fact that the correcting mechanisms for mutations are not full proof, suggests that mutations are meant to be something that can create fitter and more complex life.
Not necessarily. You are actually acknowledging that occasionally an error gets through. But you are forrgetting it is still an error. Errors are not normally associated with making something better and fitter but rather making something less fit and broken. Can you see how it does not make sense and you have to appeal allowing something illogical to happen?

Whereas if we consider there are other mechanisms that do allow change to happen but are more directed and therefore don't have to risk harm but are targeted at changes needed for adaption this makes much more sense and there is evidence for this so it is not conjecture. This does not deny evolution but gives it a better foundation rather than having to appeal to something that just does not make sense nor has scientific empirical support.
 
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stevevw

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Incorrect, with a couple of caveats. First, in a very small population of nonrecombining organisms, Muller's ratchet can take over and the accumulation of deleterious mutations rapidly drives the population to extinction. Second, when a population's size decreases, purifying selection becomes somewhat less effective, and mildly deleterious mutations can accumulate until a new equilibrium is reached.
So you are saying that apart from smaller populations slightly harmful mutations do not accumulate. From what I have read it seems they do and there are different reasons why natural selection may not be able to weed them out. For example

Despite the current status as the dominant organism on earth, the human species is confronted with substantial mutational challenges imposed by at least three baseline genetic features: (i) a relatively high per-generation germline mutation rate at the nucleotide level; (ii) a further inflation in the mutational rate of production of defective alleles associated with aspects of gene structure; and (iii) a large cumulative burden of somatic mutations imposed by a relatively late onset at maturity.
Rate, molecular spectrum, and consequences of human mutation

Every time a cell divides, genetic errors can occur, leading to variations in the DNA sequence that may proliferate and—in some cases—cause disease. Now that genetic sequencing and other technologies have made it easier to recognize mutations that occur in only a subset of cells, researchers are finding more and more harmful mutations hidden among unaffected cells.
Harmful mutations can fly under the radar

The relentless accumulation of deleterious mutations is primarily due to the existence of un-selectable “nearlyneutral” mutations, but the genetic load problem is greatly amplified when mutation rates are high. Intensified natural selection only marginally slows the accumulation of deleterious mutations.
http://bioinformatics.cau.edu.cn/lecture/chinaproof.pdf
Your disagreement is with reality, then, because random mutations really do make organisms fitter and create new complexity.
How do you know it is random mutations that are the cause of all this variety and complexity that makes living things fitter and it is not the result of other processes as mentioned below.

Everything in the EES also ultimately relies on random mutations being filtered by natural selection to produce adaptation.
I've read just about all of the EES people, and I haven't seen anything proposed as a source of adaptive evolution that doesn't end up relying on random mutation and natural selection.
This is where I tend to disagree and perhaps because some people are under the impression that the mechanism associated with the Evolutionary Extended Synthesis (EES) can be explained away through the MS theory causes them to not give enough consideration or credence to it. The basis for the EES processes is that it much of the processes bypass the need for random mutations and in many cases reduces or eliminates the need for natural selection.

For example, all phenotype variation in the Modern Synthesis (MS) stems from gene change in individual creatures. Whereas phenotype accommodation can precede, rather than follow, genetic change in the EES. This cuts out random mutations as being the cause of all variation as the form change is not genetic in the first place. Also, in the MS mutations and therefore phenotypic change will be random whereas in the EES phenotypic change will often be non-random directed, well suited and integrated. Being directed, well suited and integrated minimizes the role of natural selection is reduced because the variation is already suitable and integrated and selects itself.

In the MS isolated random mutations that cause phenotypic changes to happen in individual creatures whereas in the EES phenotypic changes are frequently environmentally induced and happen in multiple creatures. Adaptive evolution under the MS typically proceeds through the selection of small random mutational changes because larger ones have disruptive pleiotropic effects. (they undermine what is already a finely tuned setup emphasis added). Whereas under the EES large and different phenotypes can occur quickly. This can explain a lot of the sudden appearance of well-formed creatures in the fossil records. (because they use existing development programs which are designed to accommodate these changes and therefore are well integrated and don,t disrupt the current status, emphasis added).

This can happen through changes in major regulatory control genes which are expressed in a tissue-specific manner, module- or compartment-specific manner, or when developmental processes respond to environmental challenges with the change in coordinated suites of traits, or through nonlinear threshold effects (facilitated variation). Also, under niche construction creatures can change their environment rather than be changed to an environment through random mutations and natural selection. This eliminates the need for random mutations and natural selection as creatures are the ones dictating what happens. Creatures can control what happens to them rather than only being subject to adaptive evolution.

Another difference is that rather than the inheritance of genes through random mutations in the MS under the EES inheritance of traits extends beyond genes which eliminate random mutations. This includes (transgenerational) epigenetic inheritance, physiological inheritance, ecological inheritance, social (behavioural) transmission and cultural inheritance. These acquired characteristics can play evolutionary roles by biasing phenotypic variants subject to selection, modifying environments and contributing to heritability. So selection is still involved but rather than having to sift through untold random mutated variations it is handed variations already integrated and directs evolution towards certain outcomes which dreduces selections role.

Under the MS evolution is defined as the change in gene frequency, populations evolve through changes in gene frequencies brought about through natural selection, drift, mutation and gene flow. The EES takes the organism-centred perspective. Developmental systems can facilitate adaptive variation and modify selective environments. Evolution redefined as a transgenerational change in the distribution of heritable traits of a population. There is a broadened notion of evolutionary process and inheritance. Under the MS macro-evolution is explained by micro-evolutionary processes of selection, drift, mutation and gene flow whereas under the EES additional processes such as developmental bias and ecological inheritance, help explain macro-evolutionary patterns and contribute to evolvability.
About the EES - Extended Evolutionary Synthesis

Also, mutations can be non-random which implies that some mutations are part of a mechanism that living things were designed to have which allows them to alter their existing genetic material in order to adapt to environments. The environmental pressures they are under trigger targeted mutational changes in specific locations of the genome according to the particular environment pressures they are under. In other words, it allows creatures to gain the right phenotypic change for the situation they are in rather than through random mutations being blindly sorted through natural selection. If the phenotypic change is targeted and well suited then how can natural selection play much of a role when it has already been determined to be the best option available.
http://www.youtube.com/watch?v=qTChu5vX1VI

So as you can see it is not as simple as only explaining variations as coming from random mutations and natural selection being the only driving force that directs evolution. There is a raft of other processes that can reduce and eliminate the need for random mutations and natural selection which are often overlooked and even dismissed at the expense of explaining everything is gene-centric and adaptive terms. Some say that these processes are not just an extension of the current theory but are reconceptualizing evolution altogether. For me, processes incorporated in the EES and the like make much more sense in the light of recent and current evidence and explain a lot of the anomalies that the MS theory cannot account for.
 
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Job 33:6

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First off I noticed you did not address what was said about non-random directed mutations being a source of variation rather than random mutations which is the main source of variation for neo Darwinism.

I am not being specific about what level of mutation that causes fitness loss as there is contention about this. The range of mutations being passed on to each generation is said to be from around 60 to 300 mutations. There is a debate about neutral mutations having no effect on fitness as they slightly change existing sequences and therefore take up space which then requires more energy for an organism to accommodate hence a fitness cost. Given enough buildup and they begin to have a cost to fitness. Mutations do not always act in isolation so a slightly harmful change in one nucleotide can also be linked to others throughout the DNA and therefore can hard to eradicate.

As seen with recent research humans are accumulating many slightly harmful mutations and natural selection cannot keep up in purging them out of our genomes so therefore we have a building number of diseases. Beneficial mutations are said to also come with a cost as they also reduce genetic function with any perceived benefit they give. Evidence shows that the more mutations are added the more the cost to fitness regardless of what type of mutation including beneficial mutations through epistasis. So it is not as simple as claiming there are only certain situations where mutations can cause harm and where natural selection can purge out these harmful mutations.

"random mutations are basically an error in what is already working good and the fact that the DNA has a mechanism to correct those errors shows that mutations are not meant to be something that can create a fitter and more complex life. "

So, it is acknowledged that mutations are an error to what is already fit and working well but somehow some got through and still increase fitness.

Even if we believed that we would need a multitude of beneficial mutations at only 1% of all mutations to get the level of variety and complexity we have today. If that's the case we would also need an overwhelming amount of harmful mutations as well. Under normal circumstances this level of mutations is associated with sickness, malfunction and cancer let along creating something fitter.

Not necessarily. You are actually acknowledging that occasionally an error gets through. But you are forrgetting it is still an error. Errors are not normally associated with making something better and fitter but rather making something less fit and broken. Can you see how it does not make sense and you have to appeal allowing something illogical to happen?

Whereas if we consider there are other mechanisms that do allow change to happen but are more directed and therefore don't have to risk harm but are targeted at changes needed for adaption this makes much more sense and there is evidence for this so it is not conjecture. This does not deny evolution but gives it a better foundation rather than having to appeal to something that just does not make sense nor has scientific empirical support.

You're still not making a clear argument, you're just randomly speaking.

The only meaningful statement I could pull from the above is this:

"Errors are not normally associated with making something better and fitter but rather making something less fit and broken. Can you see how it does not make sense and you have to appeal allowing something illogical to happen?"

The word "mistake" implies sentience. Like someone doing something wrong and saying "oops" afterwards. I made my statement knowing that it was conjecture in hopes that you would see that yours is conjecture as well.

I would not call random mutations mistakes.
 
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Job 33:6

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"First off I noticed you did not address what was said about non-random directed mutations being a source of variation rather than random mutations which is the main source of variation for neo Darwinism."

There's no substance here. Just you asking for a response to an unclear claim.

"I am not being specific about what level of mutation that causes fitness loss as there is contention about this."

Ok, you're still not saying anything.

"Mutations do not always act in isolation so a slightly harmful change in one nucleotide can also be linked to others throughout the DNA and therefore can hard to eradicate."

Still not getting anywhere.
 
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