stevevw
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No, that's wrong. The new enzyme wasn't created de novo, but was a modification of an existing enzyme. There was no "reactivation"; the enzyme gradually became efficient at catalyzing the substrate over a period of and countless mutations, only a few of which led to the new enzyme.
It appears that the ability for humans to tolerate milk is an example of niche construction. All humans are able to tolerate milk as infants, but this ability is gradually shut down in adults. That is why I mentioned it was a reactivation of a previous ability. If humans were once able to tolerate lactose as a baby, then it seems possible that this ability was already there. In fact, scientists now call this lactose persistence rather that lactose intolerance because it is the persistence of lactose tolerance after infancy rather than the switching off that enables humans to tolerate milk. It seems lactose intolerance is the result of a loss of function in the part of the gene that produces lactase that once enabled humans to tolerate lactose.
But what is interesting is that the ability to be able to tolerate milk came at the same time humans moved from hunters and gatherers to farmers and the use of dairy products. But some people are more able to tolerate milk than others and this seems to be more prevalent in European populations that practiced dairy farming in the last 5 to 10 thousand years. But the use of milk has been attributed more to cultural practice than a matter of an adaptation.
This is an example of niche construction in that humans who tolerate lactose have created the environment to be in a better position to tolerate lactose. This happened in a couple of different locations with similar results in a fairly quick succession. It seems too much of a coincident that this happened more than once with similar results if this was purely the result of a random and blind process. It seems that because humans had put themselves in the position of using dairy products more and gaining a benefit from them that this pressure activated the component of the gene regulator to increase lactase. A good example of the environmental conditions acting on a creature’s tissues and cells to activate change.
Evolution of lactase persistence: an example of human niche construction
Lactase persistence is one of the clearest examples of niche construction in humans. Lactase is the enzyme responsible for the digestion of the milk sugar lactose and its production decreases after the weaning phase in most mammals, including most humans. Some humans, however, continue to produce lactase throughout adulthood, a trait known as lactase persistence.
Evolution of lactase persistence: an example of human niche construction
Lactose intolerance is the inability to metabolize lactose, because of a lack of the required enzyme lactase in the digestive system. The normal mammalian condition is for the young of a species to experience reduced lactase production at the end of the weaning period (a species-specific length of time). In humans, in non-dairy consuming societies, lactase production usually drops about 90% during the first four years of life, although the exact drop over time varies widely.[86] However, certain human populations have a mutation on chromosome 2 which eliminates the shutdown in lactase production, making it possible for members of these populations to continue consumption of raw milk and other fresh and fermented dairy products throughout their lives without difficulty.
this adaptation is accomplished by a loss of genetic information. The “novel” ability is acquired by a mutation that shuts off the capacity for production of the enzyme lactase.
https://evolutionnews.org/2011/12/fact-checking_w/
Also, it seems that other reserach shows that it is very hard for prteins to evolve a new function in general.
Estimating the prevalence of protein sequences adopting functional enzyme folds.
The prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10(77), adding to the body of evidence that functional folds require highly extraordinary sequences.
Estimating the prevalence of protein sequences adopting functional enzyme folds. - PubMed - NCBI
What I also find interesting is that you say that the bacteria was able to evolve irreducible complex systems which is more of a ID claim. I don't think Darwinian evolution has ever been able to show that it can evolve this.
Ok I am not too familar with this. All I know is it seems that lactose intolerance is the gradual switching off of the genes ability to produce lactase and for some, it is not switched off through a mutation. But there is nothing new here and it is all to do with the tampering of existing genetic info. The genes that may do things in a entirely different way may be just the genes ability to be expressed in many different ways. But that expression is linked to the existing ability of the genomeperhaps hold that information is some way. There is a lot of non-regulatory DNA we do not know much about how it functions.Darwin's great discovery was that it isn't random.
It wasn't. But some are more fit than others. That's the one that eventually evolved. Was it constrained to a specific path? No. This is why the genes in different taxa may do the same things, but do it in entirely different ways. Would you like to see some examples?
Adaptive Mutagenesis at ebgR Is Regulated by PhoPQ
But this does not take away from the fact that there are processes such as through development, niche construction that add a variation that is confined to specific changes and is directed to a specific path. Therefore natural selection is restricted in what it can and cannot do. This begs the question of how much of a role Darwinian processes play in the overall scheme of things. If there are many other mechanisms that produce variations then this only proves that Dawinian evolutionary processes are a small part of something bigger and have been over stated as being the only way life can change.
I don’t mean vary no more as in it will stay one form only. We know animals can change to different forms. Dogs for example can change to many different shapes but it is within a certain limit and they cannot evolve to be as large as say a cow for example. Or they cannot vary their heads to be out of proportion to their bodies. There is a limit to its size.Can you show us an organism that is at that limit, and can vary no more?
The fact that developmental programs have set forms that they conform to shows that there are limits. IE a limb will adapt to within the proportion of the body that carries it. The body plans produce certain forms over others such as 5 digits in mammals and not 6 or 4 etc. The bird beak size and shape are within limits at least functional ones are that allow them to survive. But you will not see say a 12-inch beak on a Finch. It seems strange that the beaks produced were all beneficial and happened so quick. Darwinian processes would have taken longer and produced many non-benefical beaks that had all sorts of shapes, that is the nature of random mutations. If they only conformed to certain beaks then this shows there were other mechanism at play that restricted the outcomes.
The evidence comes from what I have already been posting with the processes of the EES. Every change in form that you have presented can be explained through the processes presented in the EES. A change in head shape due to an environmental pressure can come from developmental processes such as plasticity. As mentioned, the environmental pressure can trigger phenotypic changes through effected cells and tissues for which the pressure is being exerted on. So that is why the change in form is specifically related to the change in environment or the way the a creature lives and the pressures they are under.Show us your evidence for that.
Show us those mechanisms.
It is almost similar to what people said about Lamarckian influences such as with the Giraffe example. How the Giraffe had to stretch their neck to reach leaves on trees and this led to pressure on their bodies which facilitated a change in developmental programs for the length of neck. Though the EES process is not Lamarckian but more to do with Evo Devo and epigenetics.
As previously mentioned some variations through the processes explained in the EES such as developmental processes like developmental bias, plasticity, niche construction and inheritance beyond genetics can produce adaptive variations. That is because the creature lives in tune with their environment and they are not separate entities. Phenotypic variation can happen directly through the pressures a creature is under acting on their physical makeup that will determine how genes are expressed. Or through the way a creature lives and places themselves and their offspring in positions that create more adaptive environments that will contribute to phenotypic adaptive outcomes.Starvation, for example. Selective pressure is indeed what made those changes. But show us your evidence that the only changes in the population were adaptive ones. When we observe this sort of thing, as the Grants did on Daphne Major, various changes occured, but only those with the advantageous variations lived long enough to reproduce.
What I would like to know with any variation that does not prove viable is that how do we know that the beneficial variations are not the result of re-existing genetic info that is being utilized and the non-beneficial variation is just a random mutation of what was already good. So non-beneficial mutations are just a by product of random mutations and random mutations never produce anything of benefit. There has to be some pre-existing genetic info there to get those new beneficial shapes of beaks. It seems too much a coincident that the beneficial variations of beaks happened so quick and at the right time and in the right place to all be the result of random mutations and blind selection.
Another way for creatures to gain more genetic variety to vary features is from HGT and hybridization. According to this paper the Finches have a history of hybridization which could explain how the genetic info for different beaks spread. But notice that the modern variations relate to the mixing of Finches with those beaks from previous generations through hybridization. So, the genetic info for those beaks was introduced into the gene pool and this is a case of the birds tapping into pre-existing genetic info through developmental processes. These form changes were perhaps triggered by environmental pressure triggering the genes for those beaks shapes to happen through the developmental process.
Evolution of Darwin's finches and their beaks
The following paper seems to support what I am saying. It shows that the genetic info for beak shape is already there and that the genes for different beak shapes is switched on and off through developmental processes.
Researchers at Harvard Medical School have taken the story one step further. Using modern genetic analyses, they found a molecule that regulates genes involved in shaping the beaks of Darwin finches. “Calmodulin is a protein that binds and activates certain enzymes, which triggers a signal that eventually turns specific genes on or off,” explains Arkhat Abzhanov, an evolutionary biologist at Harvard. These signals alter the behavior of cells responsible for beak sculpturing.
How Darwin’s finches got their beaks
It may not be that all variations are the produce of random mutations and that natural selection is winnowing all these variations into certain forms for adaptive reasons alone. Under this scenario we would end up with a lot of excess baggage that proves unnecessary and non-beneficial. This black and white scenario which is fixated on genes, adaptations and gradual change alone seems too restrictive to what we see. It appears that the variations can have a wide range but most if not, all are of some benefit and belong.
They are all produced through develop and in response to changing environments which just shows the incredible connection between creatures and ecosystems. It’s almost as though they are an extension of their environmental rather than a separate entity trying to fit in in a case of live or die. It may be that there just a vast amount of variation within the natural genetic makeups of life. Any truly non-beneficial change is the result of contamination of the genome by truly random mutations that alter the original state.
Yes but Darwinian processes seem to be hit and miss and some of the changes we see are specifically guided and produce the right forms relatively quick, perhaps too quick for Darwinian evolution.So Darwin showed us.
Which can also be the same for just about any living thing. So how does this fit in with Darwinian evolution that shows no direct connection between environment and phenotype in the sense that the environment cannot trigger a specific variation that proves adaptive. The right adaptations according to Darwin’s theory come from a hit and miss process where the production of many random variations will produce a rare benefit that proves adaptive.Which is most often, the same as changes in human physiology, depending on altitude.
I think this is a matter of interpretation. What is determined as a beneficial variation from a random process was actually a well suited and integrated variation from a developmental process tapping into a pre-existing genetic info for that variation. That is what the EES is beginning to expose that what has been assumed to be Darwinian processes has actually been the result of other more self-organised and directed processes.As the Grants demonstrated, this works very well.
I am not saying Natural selection does not play a part, just that it has been over stated and this is supported by the many links I have posted saying this. Even though eukaryotes are a symbiotic event from simplier organisms it seems the symbioctic even itself was not something that was random. It was compliemntary in the sense that it was a natural extension of single celled life and could not have happened any other way. So in that sense it seems there are other laws and codes that govern how this happens rather than being a totally random occurance.It's not a crazy idea; eukaryotes are symbiotic organisms. But natural selection mediates that process; it's been directly observed:
Even a staunch evolutionist like Micheal Lynch states that the evolution of complex life was not the result of natural selection. Complex organisms seem to be the result of non-adaptive mechanisms rather than adaptive ones.
What is in question is whether natural selection is a necessary or sufficient force to explain the emergence of the genomic and cellular features central to the building of complex organisms.
The frailty of adaptive hypotheses for the origins of organismal complexity
The same with Koonin.
Evolutionary-genomic studies show that natural selection is only one of the forces that shape genome evolution and is not quantitatively dominant, whereas non-adaptive processes are much more prominent than previously suspected. Major contributions of horizontal gene transfer and diverse selfish genetic elements to genome evolution undermine the Tree of Life concept. An adequate depiction of evolution requires the more complex concept of a network or ‘forest’ of life. There is no consistent tendency of evolution towards increased genomic complexity, and when complexity increases, this appears to be a non-adaptive consequence of evolution under weak purifying selection rather than an adaptation.
Darwinian evolution in the light of genomics
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