The Fossil Record Proves Speciation, Not Evolution of Lifeforms Observed

[Justatruthseeker]

Why not settle, arguendo, for the definition provided by Christian Forums?

And so then how do you detect the wolves in sheeps clothing? Because the wolves also lay claim to the title.

 

[Speedwell]

And so then how do you detect the wolves in sheeps clothing? Because the wolves also lay claim to the title.

A person who insists on laying claim to the title probably doesn't deserve it.

 

[Justatruthseeker]

That’s true but is only highlighting the harmful effects. Common mutational changes are usually deleterious or neutral. The paper as with most papers on this topic do not state exactly what function needs to be changed. They are talking about any functional change that will be functional that requires more than one mutation.

Their research is talking about the need for replacing two or more specific nucleotides changes for a new specific function that will require two or more linked mutations. It is also not just about the right mutations in the right place but about their amplification and fixation which can also take a long time.

Frameshift mutations result in abnormal protein products with an incorrect amino acid sequence that can be either longer or shorter than the normal protein. They are not talking about any single or double mutation substitution but a new functional change that requires multiple dependent mutational change. This does not have to be in one generation.

If a single substitution happens to have little effect, then it is of no benefit for a specific function change. Therefore, additional linked mutations need to happen and not another unrelated single mutation. Most single unrelated frameshift and substitution mutations are harmful, effect function of proteins or have no or little effect.

The authors gave a 10% reproductive fitness benefit to amplify the selective benefit when single substitution was added to the target string. So, in reality their results are underestimated. The tests also disregarded other factors that could interfere with the success of establishing these mutational changes such as selection interference from other mutational changes in other parts of the genome which would add more time.

View attachment 235472

Each value is the mean of 25 replicates. The population (10,000) and beneficial fitness effect (10 %) were held constant. The mutation rate was adjusted based on number of nucleotides in the string. For single point mutations (string length of one), numerous instances accumulated simultaneously in the population – such that many were superfluous to waiting time, resulting in extra instances arising prior to fixation.

Table 2 also shows the waiting times for creating and fixing genuine strings of 2–8 nucleotides. This data is also plotted in Fig. 2. Each additional nucleotide that was added to the target string substantially increased waiting time. Figure 2 shows that as string length increased linearly, the increase in waiting time was of an exponential nature. When there were as many as six nucleotides in the string, the average waiting time (4.24 billion years) approached the estimated age of the earth. When there were eight nucleotides in the string, the average waiting time (18.5 billion years), exceeded the estimated age of the universe.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/#CR15

It is not my claim but the scientific results of the work of scientists. I am not saying that specific functional gene change cannot happen. I am just saying that this may not happen by a Neo-Darwinian process of random mutations and natural selection, but rather other processes mentioned in the EES which seem to make more sense.

But if two mutations need linked over time to produce a beneficial result, then why would the body continue to preserve and waste energy on an appendage that is non functional?

From some point from development from flippers to legs, it neither grants advantage to water travel or land travel, but is in fact a hinderance to both. It is working against survival. This is the problem that must be overcome not once, but billions of time in the mutational view. At every stage there is a point lasting unknown eras where the mid-development is working against survival, not for it.

 

[Speedwell]

But if two mutations need linked over time to produce a beneficial result, then why would the body continue to preserve and waste energy on an appendage that is non functional?

From some point from development from flippers to legs, it neither grants advantage to water travel or land travel, but is in fact a hinderance to both. It is working against survival. This is the problem that must be overcome not once, but billions of time in the mutational view. At every stage there is a point lasting unknown eras where the mid-development is working against survival, not for it.

Yes, that is exactly the "straw man" we're talking about. Thank you for giving us such an easily understandable example of creationist perfidy so we can better explain the idea to Steve.

 

[tas8831]

They are talking about a specific functional change that may require linked multiple mutations on the same short DNA over several generations. Therefore the mutations will not be any mutational change on any place in the genome but a specific mutational change that needs to be made that is needed to produce a change where more than one mutation is needed.

This is post hoc strawmanning.

 

[tas8831]

But if two mutations need linked over time to produce a beneficial result, then why would the body continue to preserve and waste energy on an appendage that is non functional?

LOL!

Are an ostrich's wings functional?

From some point from development from flippers to legs, it neither grants advantage to water travel or land travel, but is in fact a hinderance to both. It is working against survival. This is the problem that must be overcome not once, but billions of time in the mutational view. At every stage there is a point lasting unknown eras where the mid-development is working against survival, not for it.

So precious...

So why did your deity 'design' things that way?

I love how YECs continually argue against their own dopey claims without realizing it.

 

[tas8831]

Because from any given starting point there are so many possible functional outcomes, not just the one which happened to develop.

Indeed.

It is like rolling a pebble down a hill - it may or may not reach the bottom. If it does, there are any number of paths it could have taken. The arguments Behe and Snoke and steve and Sanford are making is that because the pebble reached the bottom, it is impossible to have done so by chance because it needed to take the path it did.

 

[tas8831]

Those rare beneficial mutations have to be the right ones in the right place that will be related to the specific change needed.

This is funny - to actually see in writing a clear as day example of a strawman laid out like this with not so much of a hint of awareness.

Way to imbue a natural process with teleology and then wonder why the natural conundrum is not explained...

 

[stevevw]

Because from any given starting point there are so many possible functional outcomes, not just the one which happened to develop.

This does not make sense. In your previous reply you say

Speedwell says
Yes, the odds of a particular series of mutations leading to a particular functional outcome are very small. Everybody agrees to that. But the odds of a series of mutations leading to some functional outcome are actually quite favorable.

On the one hand you say the odds of a particular series of mutations leading to a particular functional outcome are very small. Then you contradict this by saying the odds are very favourable for the same thing to happen.

How do we know that these functional outcomes are the result of Darwinian evolution and or from other processes such as with the EES and the like. It is an assumption that there are so many functional outcomes from the evolution of particular combinations of mutations becuase the assumption that is Darwinian processes that are responsible has already been made therefore circular reasoning.

There are also many more non-functional possibilities as well and considering that proteins are very specific in their structures and the vast non-functional possibilities I would say the odds are not as great as you make out.

 

[Speedwell]

This does not make sense. In your previous reply you say

Speedwell says
Yes, the odds of a particular series of mutations leading to a particular functional outcome are very small. Everybody agrees to that. But the odds of a series of mutations leading to some functional outcome are actually quite favorable.

On the one hand you say the odds of a particular series of mutations leading to a particular functional outcome are very small. Then you contradict this by saying the odds are very favourable for the same thing to happen.

Not for the same thing to happen. Not for a particular functional outcome, but for any one of the many other possible functional outcomes which may be reached from that same first "mutation."

How do we know that these functional outcomes are the result of Darwinian evolution and or from other processes such as with the EES and the like.

That's a hard question, because most of us don't divide evolution into "Darwinian" and "EES" processes like you do. Let's just say that random variation is mostly random or it wouldn't plot to a bell curve like it is most often observed to do.

 

[stevevw]

Indeed.

It is like rolling a pebble down a hill - it may or may not reach the bottom. If it does, there are any number of paths it could have taken. The arguments Behe and Snoke and steve and Sanford are making is that because the pebble reached the bottom, it is impossible to have done so by chance because it needed to take the path it did.

Biological information is completely different to Shannon info. Comparing this to there being several paths down a hill is too simplistic and perhaps shows how some try to simplify things so that they can account for what we see which has proven very hard to explain by this logic. AS I said if mainstream biologists use the same hindsight logic to calculate the chances then they are also perpetrating the wrong idea about evaluating evolutionary processes.

As far as I can see this method of looking back and trying to evaluate what processes and how it happened occurs in just about every field of science from archeology to astrophysics. They do exactly the same thing in beginning with assumptions about how things happened and then mapping out how it actaully happened according to those assumptions.

 

[Speedwell]

Biological information is completely different to Shannon info.

Why?

Comparing this to there being several paths down a hill is too simplistic and perhaps shows how some try to simplify things so that they can account for what we see which has proven very hard to explain by this logic. AS I said if mainstream biologists use the same hindsight logic to calculate the chances then they are also perpetrating the wrong idea about evaluating evolutionary processes.

Not if they make the distinction between the odds of a particular favorable outcome and the odds of any one of all possible favorable outcomes.

As far as I can see this method of looking back and trying to evaluate what processes and how it happened occurs in just about every field of science from archeology to astrophysics. They do exactly the same thing in beginning with assumptions about how things happened and then mapping out how it actaully happened according to those assumptions.

But they don't assume--as you appear to do-- that it was the only thing which could have happened.

 

[tas8831]

Then why is it not only what you say are creationists doing the research and debating about the probabilities of evolution evolving specific mutations that are needed for a specific function but also mainstream scientists. They respond to what Behe says and say that his calculations are wrong and then go about setting him strait on the very same scenarios by looking back at the probability of this happening.

I am curious if you have actually read the paper you keep referring to and quoting. I see you keep quoting it, yet you seem to keep misrepresenting it. It wouldn't surprise me - creationists have a history of merely copy-pasting quotes from papers they have read on YEC websites and citing them as if they had actually read it. Had a creationist on a different forum copy-past a quote from a book from a YEC website - complete with ellipses and truncated sentence. When I provided that exact quote on 4 or 5 different YEC sites, then provided the entire quote from the actual source, he still insisted that he had read the original source and that the quote was in fact his own. When it clearly wasn't.

I ask because you left off the end of that section, which lays low your premise:


"In addition, we use these results to expose flaws in some of Michael Behe's arguments concerning mathematical limits to Darwinian evolution."


And earlier in your quote, we see:


"In particular, we examine the waiting time for a pair of mutations, the first of which inactivates an existing transcription factor binding site and the second of which creates a new one."

But you did not highlight that for some reason. Do YOU suppose this is the main manner in which evolution proceeds? By the deactivation of one binding site and subsequent activation of a new one? Do you suppose that ANY evolutionary biologist/population geneticist believes that this is the main or only way evolution proceeds? Because the dogged manner in which you keep harping on this tells me that you DO think this.

Allow me to explain why I don't really care much about this whole topic, as it pertains to 'problems for evolution' -

Hillis et al. published a series of very nice papers in the 1990s testing the validity and accuracy of the use of molecular phylogenetic techniques. In one of their papers, they wanted to basically test the limits of the techniques. They propagated their experimental virus in a high mutation environment (not natural) and sequenced regions of the genomes of viruses in each 'generation.' The results of these extreme tests showed that in such un-natural, high mutation rate environments, looking at the small genomes of viruses with no mutation repair mechanisms, the results of molecular phylogenetics analyses were inconsistent. This paper was, of course, pounced on by the usual suspects as PROOF! that such techniques were totally unreliable and can be ignored.

When I read your posts on this 'waiting for 2 mutations' thing, I get much the same impression.

You also seem to have missed a major premise - in the case of cancer,which was the impetus for the D&S paper, if the 'waiting time' thing had merit, then how is it that so many people develop cancer? I should also note that they are specifically looking at changes in regulatory sequence, not protein-coding genes - you saw that, yes?

Some end up coming to the same conclusions as what Behe and Sanford has shown. For example Durrett and Schmidt are mainstream scientists publishing in mainstream Journal GENETICS state

Results of Nowak and collaborators concerning the onset of cancer due to the inactivation of tumor suppressor genes give the distribution of the time until some individual in a population has experienced two prespecified mutations and the time until this mutant phenotype becomes fixed in the population. ... but for humans with a much smaller effective population size, this type of change would take >100 million years.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581952/

100 million years far exceeds the 6 million years it took for apes to become humans.

If only the transition from ape-ancesor to human 100% relied on 2 pre-specified mutations in regulatory sequence occurring one after the other...

Are you familiar with the concept of an academic exercise? See my anecdote about Hillis and the viruses above.


As an aside - a thought experiment of sorts - if, as you like to quote, the 'waiting time' in humans in more than 100 million years for 2 pre-specified mutations to occur, and that sentence was in response to the 2 pre-specified mutations causing cancer getting fixed in the population, then should it not be the case that NO humans have cancer?

Do you see what the issues are? Because it seems to me that you do not.

 

[tas8831]

Biological information is completely different to Shannon info.

Really? Do tell. Because whenever I have written this in the past, anti-evolutionists tell me that I don't understand.

But as you are now presenting yourself as an "information" expert, perhaps you can explain if a gene duplication counts as an increase in information.

Comparing this to there being several paths down a hill is too simplistic and perhaps shows how some try to simplify things so that they can account for what we see which has proven very hard to explain by this logic.

Isn't it odd - I use a simple analogy to make a point, and the creationist, excuse me, not a creationist has a fit.
Well please explain how my analogy does NOT represent the arguments that Sanford and Behe and you are putting forth.

AS I said if mainstream biologists use the same hindsight logic to calculate the chances then they are also perpetrating the wrong idea about evaluating evolutionary processes.

Yes, YOU said that. But you failed to see why these 'mainstream biologists' are discussing it. I sincerely doubt that any mainstream biologists think that evolution proceeds solely via a series of 2 pre-specified mutations occurring in regulatory sequence. Unless you have examples?

As far as I can see this method of looking back and trying to evaluate what processes and how it happened occurs in just about every field of science from archeology to astrophysics. They do exactly the same thing in beginning with assumptions about how things happened and then mapping out how it actaully happened according to those assumptions.

And when their assessments demonstrate that their models do not comport with reality, then only creationists cling doggedly to them at all costs. D&S took the assumptions of others and applied them to the Behe assertions and showed how silly they were.

Guess you missed that part.

 

[tas8831]

This does not make sense. In your previous reply you say

Speedwell says
Yes, the odds of a particular series of mutations leading to a particular functional outcome are very small. Everybody agrees to that. But the odds of a series of mutations leading to some functional outcome are actually quite favorable.

On the one hand you say the odds of a particular series of mutations leading to a particular functional outcome are very small. Then you contradict this by saying the odds are very favourable for the same thing to happen.

I strongly suggest you go back and re-read Speedwell's statement and your 'summary' of it. You are misrepresenting what he said.

 

[tas8831]

The more molecular biology we learn the more we see such new information does not support the foundation that living things have evolved.

All of the biochemistry about even physiological diseases (particularly neuropathic of spine and brain) the complexity displays multiple mutations in sequence and time in order for the known physiological cause to exist. No one single mutation can account nor continue without the string of other mutations for such said complex physiological "systems" of biochemical interactions and intergrations to exist.

As usual - lots of baseless assertions, nothing of substance.

Still waiting for you to admit that you have never looked at a fossil.

 

[stevevw]

Not for the same thing to happen. Not for a particular functional outcome, but for any one of the many other possible functional outcomes which may be reached from that same first "mutation."

That is putting a different context on things and widening the scope of what is being analysed. They are talking about these specific changes requiring specific mutations in a small section of DNA and not the entire genome.

If we take an overall view and look at the genome and say there are many possible sites for specific functional change in sequences that would be true. But we are not specifying things. When we look at a particular site and what is involved it then changes the criteria and more specific info is needed. Each and every site change will demand that same level of analysis and explanation.

Despite there being many possible functional outcomes each and everyone has a spepcific set of processes to achieve this. When you look at this in the context that there are many more non-functional possibilities this shows that in reality despite whatever outcome you want to look at there is still only a very narrow window of possible functional outcomes.

That's a hard question, because most of us don't divide evolution into "Darwinian" and "EES" processes like you do. Let's just say that random variation is mostly random or it wouldn't plot to a bell curve like it is most often observed to do.

I am not the only one who supports the EES processes and there is a growing number of scientists who do. This is part of the problem. By not determining how variation is produced you would not know and therefore because people assume that it is derived from Neo-Darwinism (random mutation) their results will also be based on assumptions. This will taint the way they see things and influence the outcomes. IE if variation or a particular change in function is caused by a development process (development bias or plasticity) that is directed will be seen as random and the result of Darwinian processes.

The bell curve is not well suited to biological info and cannot determine random and non-random processes. Many results of non-random variations can appear random because each individual creature is subject to different conditions. Plasticity can produce varying phenotypes that are no based on gene change and therefore have no effect on survivability. Other factors associated with extra genetic inheritance and niche construction can appear random because individual living things are subject to different environmental conditions and may also respond differently in how they change but still achieve the same end result.

In reality, most biological data do not conform to a perfect bell-shaped curve, and, in some cases, they may profoundly deviate from this ideal.
http://www.wormbook.org/chapters/www_statisticalanalysis/statisticalanalysis.html[/QUOTE]

 

[tas8831]

Some have displayed what they think are transition fossils showing morphological changes. The did not truely present a succession of morphological changes in the fossil record over time. Only macro-assemblages that weere force fit to align into a scheme of "features evolved".

As you are self-proclaimed expert on fossils and now molecular biology, please explain exactly what you think a "macro-assemblage" is and why you think that does not work as evidence for evolution.

You seem to think that there should be some fine gradation from generation to generation.

And this notion is the notion of a true novice, a person that does not understand the relationships between things like mutations and phenotype.

IOW - you are a run of the mill internet creationist, pontificating about scientific matters that you understand only enough of to make a fool of yourself.

 

[tas8831]

Some posters who like Googlism info need to first look in paleontology texts printed prior to 1970 to see how macro-assemblages were already presented as the existing evidence that the fossil record shows evolution occurred.

They knew of the massive gaps of morphological changes that had to occur between the presented macro-assemblages. But they did not have any better fossil record evidence to present.

Such as a fish fin turning into an arm-like assemblage. And eventually with a primative forked hoof or hand.

A lot of conjecture (missing evidence- and assumed reality) that such mix and match fossil features really did occur and is evidence of evolution.

Conjecture cannot be avoided by those stating the fossil record proves evolution occurred.

There is zero fossil record evidence that show evolution happened. How one lifeform changed into another lifeform over time in the fossil record.

This thread has showed many do not want to face up to this reality.

You like to yammer about these issues as if you are an expert of some kind.

Odd that you never offer any evidence for creationism.

Bible verses are not evidence, and your fake knowledge is only evidence of your desperation to prop up your failing belief system.

 

[Speedwell]

The bell curve is not well suited to biological info and cannot determine random and non-random processes. Many results of non-random variations can appear random because each individual creature is subject to different conditions. Plasticity can produce varying phenotypes that are no based on gene change and therefore have no effect on survivability. Other factors associated with extra genetic inheritance and niche construction can appear random because individual living things are subject to different environmental conditions and may also respond differently in how they change but still achieve the same end result.

In reality, most biological data do not conform to a perfect bell-shaped curve, and, in some cases, they may profoundly deviate from this ideal.
http://www.wormbook.org/chapters/www_statisticalanalysis/statisticalanalysis.html

LOL! Evidently you didn't read that paper clear though, or didn't understand it--all standard undergraduate inferential statistics.