The twentieth century unveiled the world of molecular biology, including DNA, the genetic code, proteins, and the molecular basis for modern genetics. Such findings, according to Neo Darwinists, nicely supported evolution. Evolutionary change was fueled by variation arising from genetic mutations. How the genes, and their supporting cast, arose in the first place was a more difficult question. But given their existence the evolutionary narrative was held with great confidence. This straightforward narrative is now understood, however, to be too simplistic. For instance, we now understand that biological variation often arises not from changes in the genes but rather from changes in the expression levels of the genes. Even those celebrated beaks of Darwin's finches appear to be changing via variation in gene expression levels. And more significant variation, such as body plan differences in related insects, also correlate with varying gene expression levels. These new findings do not bode well for traditional evolutionary theory.From yeast to humans, studies reveal that biological variation can correlate with gene expression levels. Interestingly, as one recent paper explains, these varying levels of gene expression repeatedly show up in some genes but not others. The mechanisms that control the gene expression levels, though varied, focus on these genes.
For instance, recent studies have found that the similar genes in similar species may have substantial differences in expression levels, while other types of genes share conserved expression levels.
In fact, varying expression levels correlate with changes even within a species. New research published this week reveals that gene expression levels can vary significantly between people who otherwise, of course, share extremely similar genomes. As one researcher explained:
the bulk of the differences among individuals are not found in the genes themselves, but in regions we know relatively little about. Now we see that these differences profoundly impact protein binding and gene expression.
In fact, not only do gene expression levels vary between related species and individuals within the same species, they also vary within the same individual, for instance in response to different environmental changes. As one evolutionist explains, when the expression of a gene is strongly regulated between different conditions, it also evolves rapidly between related strains or species. It seems the line between physiology and evolution is blurred:
Thus, it is possible that genes differ in their capacity for expression flexibility, which is manifested at various timescales: during evolution in response to mutations; during physiological responses to environmental changes; and within a population of cells as a result of stochastic fluctuations.
He concludes:
As noted above, expression divergence (the extent to which expression of a gene evolves) correlates with expression responsiveness (the extent to which expression of a gene is changed in response to the environment). We believe that the promoter elements discussed above underlie expression flexibility of these genes on short timescales (responsiveness and noise), which are instrumental in the immediate response of a cell to the environment, as well as on longer timescales (expression divergence), which may allow evolutionary adaptation to novel conditions. In other words, the correlation between responsiveness and expression divergence may be due to their dependence on the same promoter properties.
But the mechanisms that influence the gene expression levels are not simple. They involve proteins and DNA sequences. With the traditional theory of evolution we must believe that mutations created such mechanisms, one step at a time while they had little or no ability to influence expression levels. We therefore must contrive imaginary functions that would conveniently lead to their powerful expression level control capabilities.
Furthermore these expression level mechanisms needed to be applied only to certain genes. Not only are the mechanisms complex, but they must arise in the right place.
But the problems do not stop there. For such mechanisms, even when fully operational, would have limited usefulness. They must await environmental challenges to reveal their true worth. When such challenges arise the expression levels of those certain genes must change in the right way. The mechanism, if it works correctly, becomes invaluable. But until then it waits.
So now evolutionists speak of the evolvability of gene expression. The right genes, they say, have an inherent capacity to evolve its expression. In other words, evolution created the mechanisms which caused more evolution to occur—evolution creates evolution.
The orginal source is...
ReplyDeletehttp://www.sciencemag.org/cgi/content/abstract/science.1183621v1
It is not freely available yet since it just came out.
From the abstract...
"Binding differences were frequently associated with SNPs and genomic structural variants (SVs) and were often correlated with differences in gene expression, suggesting functional consequences of binding variation. Furthermore, comparing PolII binding between human and chimpanzee suggests extensive divergence in TF binding. Our results indicate that many differences in individuals and species occur at the level of TF binding and provide insight into the genetic events responsible for these differences."
I will comment about my thoughts on whether or not this is bad news for mainstream evolutionary theory later.
One thing that I don't really understand is the need to discredit every thought indicating the existence of evolution. To me, as a research fellow working with prokaryotic evolution, there is no doubt in my mind that evolution is a fact. Nevertheless there are important things that, in my view, can't be explained. One such mystery is the unexpected short time in which life came to existence (suggesting to me either design or an extraterrestrial origin). Another unknown is the origination of completely novel genes where existing theories seem inadequate. Design is certainly one possibility.
ReplyDeleteI think though in the light of the large body of evidence where nearly everything can be adequately explained by evolutionary theory it is really difficult not to believe in its existence. Do evolution and design have to be mutually exclusive?
ano:
ReplyDelete===
One thing that I don't really understand is the need to discredit every thought indicating the existence of evolution.
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I don't follow. How is it that false expectations and evidence that requires unlikely epicycles indicate "the existence of evolution"?
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To me, as a research fellow working with prokaryotic evolution, there is no doubt in my mind that evolution is a fact. Nevertheless there are important things that, in my view, can't be explained. One such mystery is the unexpected short time in which life came to existence (suggesting to me either design or an extraterrestrial origin). Another unknown is the origination of completely novel genes where existing theories seem inadequate.
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Then how can evolution be a fact? You are saying you have no doubt evolution is a fact, but you then immediately follow with the admission that fundamental claims, made in textbooks, by the NAS, in the popular literature, in journals, and so forth, are weak to the point of probably being incorrect. If you are correct, then evolution would need to be substantially revised. How then can it be a fact?
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Design is certainly one possibility.
I think though in the light of the large body of evidence where nearly everything can be adequately explained by evolutionary theory it is really difficult not to believe in its existence. Do evolution and design have to be mutually exclusive?
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According to IDers the answer is "no." According to evolutionists the answer is "yes."
Dr. Hunter,
ReplyDeleteThank you for providing an interesting intellectual cave for me to explore. I found this 2009 review article...
Aphylogenomic analysis of bacterial helix-turn-helix transcription factors
http://www.fr.embnet.org/ADE-4-old/ref/SantosFEMSMR2009.pdf
"With an astonishing capacity to survive and populate virtually every available ecological niche, the diversity of the microbial world is a fascinating living example of high evolutionary capacity. The bacterial genomes, small-sized and nowadays simple to sequence, together with their enormous diversity, are an excellent model to study both phylogenetic adaptation and ecological adaptability.
...
Adaptability is based on a set of factors that contribute to the final goal of survival through regulation, and includes modulation of transcription as one of the first lines of response. An exhaustive analysis of 145 prokaryotic genomes has unveiled the dominance of one-component systems as the main transcription factors (TFs) among prokaryotes: not only are they the precursors of the twocomponent systems, but they also present a larger diversity in terms of domains and a broader distribution among bacteria and archaea (Ulrich et al., 2005). Among the bacterial one-component TFs, up to 84% of the output domains comprise a DNA-binding helix–turn–helix (HTH) region (Ulrich et al., 2005). So, although not restricted to transcription regulation, the HTH motif assumes a central role in this process (Aravind et al., 2005). Briefly, an HTH motif consists of two a-helices forming an internal angle of around 1201 and connected by a short turn of four residues; this turn can, however, be extended to as many as 21 amino acids in the winged turns (Rosinski & Atchley, 1999). The whole structure comprises 20 residues and the second helix, known as the ‘recognition helix’, is involved in the sequence specific DNA interaction (for a review on HTH structure, see Kohn et al., 1997, and cited references). Although there is a huge functional diversity among TFs carrying an HTH domain, these regulators seem nevertheless to have a monophyletic origin, having arisen from duplication followed by divergence and specialization (Rosinski & Atchley, 1999)."
"Concluding remarks
Ecological adaptability, i.e. the capacity to perceive and to fit to transient oscillations in the surrounding environment, is crucial for survival and growth. Although the observed responses are short-term, the tools that support this resilience are part of the genetic pool of each individual. Among such tools are the one-component TFs, able to activate or repress the expression of certain genes responding to external or internal stimuli. It has been known since Darwin that evolution selects the most adapted structural features. The main question we intended to address while reviewing TFs was whether evolutionary forces were able to reshape the deep genomic features in such a way that could influence adaptability or, in other words, whether the range of conditions a certain organism can withstand is determined by the selective forces it has been exposed to through geological time. We have addressed the diversity of HTH bacterial-regulators using a statistical approach, and the outcome is consistent with the idea of multiple selective forces modulating the number and kind of regulators present in a given genome. So, recalling Haeckel, it seems that not only ontogeny, but also adaptability, recapitulates phylogeny."
It doesn't look like the authors of this article view transcription factors as a problem for evolutionary theory.
I'm still looking into this interesting subject.
Another paper...
ReplyDeleteGenome-Wide Identification and Evolutionary Analysis of the Animal Specific ETS Transcription Factor Family
http://www.la-press.com/cmr/redirect_file.php?fileId=2372&filename=1682-EBO-Genome-Wide-Identification-and-Evolutionary-Analysis-of-the-Animal-Spe.pdf&fileType=pdf
"Transcription factors (TFs) are the key regulators of gene expression at the transcriptional levels. They play crucial roles in the life cycle or biological processes of all living organisms, such as development, growth, and responses to environmental stimulus. TFs are usually classified into different families and subfamilies based on the sequence of DNA-binding domains they contain, which are highly conserved among species.1,2 Some of these families are common to most eukaryotic organisms, and some are specific to a given taxonomic group.
The ETS TF family is one of the largest families of TFs. All members of this family share a highly
conserved DNA-binding domain of 85 amino acid residues named the ETS domain. The ETS family is further sub-classified into a number of subfamilies3,4 based on the sequence similarities of the ETS domain and the presence of additional conserved domains. The ETS TFs are present throughout the body and are involved in a wide variety of functions including the regulation of cellular differentiation, cell cycle control, cell migration, cell proliferation, apoptosis (programmed cell death), and angiogenesis.4"
"Evolution of the ETS genes
We constructed the molecular phylogenetic tree of the ETS TF family for ten species of animal kingdom. The overall divergence pattern of the ETS genes appears similar to that of other gene families such as the homeobox family12 and the nuclear receptor genes.13 Laudet et al30 constructed a phylogenetic tree of the ETS gene family using 61 known ETS genes and showed the ETS TF family members can be classified into 13 groups, which could be further clustered into five subfamilies. Our classification is in general consistent with theirs.
...
Our results show the ETS genes of mammalian animals exist in both groups I and all subgroups of group II. So, we infer that the diversification of these genes predates the divergence of mammalian animals."
I think I am getting a feel for Transcription Factors and Transcription Factor genes. It appears the authors of this paper don't view Transcription Factors as a problem for evolution either.
Dr. Hunter,
ReplyDeleteI took some time to think about this thread. I even went back and read some of your old posts. I was really trying to understand things from your prospective.
If it isn't obvious by now, I can agree with your argument the complexity of life strongly suggests the need for a paradigm shift in evolutionary thinking.
I tend towards focusing on life being quantum-based.
However, I am not convinced Biologists, at large, are perpetuating a hoax and/or are clueless.
As to this Thread's opening post, I am not sure having both DNA and Transcription factors affecting biological processes is fundamentally any more problematic for evolution than DNA alone. At best, it is just additional complexity in something that is too complex already.
On the other hand, your accusation of evolution creating evolution is worth considering.
Once again, I can understand the frustration of seeing apparent self-organization emerging from “sheer dumb luck” (to quote JoeG). This is one of the reasons I look towards the self-organizing aspects of Quantum Mechanics. We do the best we can with the observations we have and make hypotheses in an attempt to make sense of it all.
If the Red Queen hypothesis of evolution is valid, then organisms which don’t evolve are at a disadvantage. (see http://ccl.northwestern.edu/netlogo/models/RedQueen).
But if the organisms blindly evolve for no good reason that could put them at a disadvantage.
What if by random, quantum or God an organism inherits a mutation which ends up causing evolution during times of stress (when changes are a good idea) but doesn’t when not stressed (when changes are a bad idea)?
Humans have an “…absence of the final enzyme (L-gulononolactone oxidase) in the pathway of vitamin C (ascorbate) biosynthesis. This enzyme was present in primitive primates, but was lost in the primate lineage leading to monkeys and apes in the Eocene (55-35 MYA). This generated a need for humans, monkeys, and other "higher" primates to obtain ascorbate from the diet.
…
Ascorbate has numerous biologic functions, including important roles in the synthesis of collagen, creatine and catecholamine. However, one of its most important roles is to function as an electron donor, or anti-oxidant. Antioxidants are thought to play a key role in the protection of species by blocking lipid peroxidation, DNA damage and alkylation, and cell membrane injury[7,8].”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2495042/
A suggestion is because of the absence of an enzyme higher primates had less “DNA damage” when times were good but mutated during the hard times resulting in better survivability.
This situation has some interesting discussion topics we could explore. Is it “religion” to suggest the absence of the same enzyme in higher primates is evidence humans, monkeys and apes descended from a common ancestor(s)?
On the other side, is the benefit derived from a genetic “defect” just too fortuitous to be a coincidence?
"A suggestion is because of the absence of an enzyme higher primates had less “DNA damage” when times were good but mutated during the hard times resulting in better survivability"
ReplyDeleteThis is not logic, if you have more rate of mutation during hard times the only thing you will got is extinction because mostly mutation are dangerous.
Hi Blas,
ReplyDeleteIf a species does not change when the environment drastically changes, it has 100% causalities and become extinct.
If under the same conditions with mutations 99.99% may die quicker but it gives the species a better chance of survival.
Something is better than nothing.
This is the kind of thing that happens in bacteria which evolve antibaterial resistance.
From PubMed...
"A nationwide outbreak of a multidrug-resistant E. hormaechei outbreak strain (EHOS) occurred in The Netherlands [14]–[16]. This strain spread throughout hospitals, despite the adequate implementation of internationally accepted infection prevention guidelines, and caused invasive infections in more than 100 patients [16]. Epidemic strains, due to their prevalence, have a greater chance of acquiring new virulence and resistance genes [17], [18].
...
In a previous study, we showed that the chromosome of the EHOS contained the High Pathogenicity Island (HPI), which most likely increased virulence of the EHOS [19], [20].
...
Three basic variants of the HPI have been described. All HPI variants contain a common P4-like integrase, called intB, and a region that encodes for an iron uptake system followed by an AT-rich sequence."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801613/
Are you going to suggest the microbiologists who wrote this don't know what they are talking about and are blinded by their indoctrination into "Darwinism"?
By the way, the title of the paper is Evolution in Quantum Leaps: Multiple Combinatorial Transfers of HPI and Other Genetic Modules in Enterobacteriaceae
The “Evolution in Quantum Leaps” in this case is due to Horizontal Gene Transfer. This kind of thing turns Darwin’s Tree of Life into more of a bush.
The point is biologists and, especially, microbiologists appear to be more than willing to move beyond Darwin if the evidence leads them that way.
Thank you Cornellius "The Darwinian" Hunter for this post.
ReplyDeleteIn fact, it only confirms the SMH proposed by John A. Davison. Its what I personally have been thinking about for years.
The following statement is a complete devastation of the Neo-Darwinian fairytale:
"biological variation often arises not from changes in the genes but rather from changes in the expression levels of the genes"
I have personally come to two testable concepts on evolution:
ReplyDelete1) continous incremental evolution (CIE)
2) discrete differential evolution (DDE)
1) is completely darwinian, changes correlate and are dependent upon individual genes via random mutations and natural selection. They are continous changes in that any change can be reverted back to its previous condition. They are incremental in that they can accumulate but the magnitude of change is restricted.
2) is completely anti-darwinian, in that changes do not correlate and are independent of random mutations and natural selection. They are discrete in that changes that occur can never be set back the same way an odometer can never be set back (unless its engineered or hacked otherwise). They are differential in that changes occur after a certain programmed condition is reached. Hence, they are restricted to the number of programmed conditions that can occur.
Mutations designing such mechanisms with precision otherwise the design cannot progress to the point where it is now is absurd. Mutation design, an error from the DNA code that can supposedly upgrade life to the specified complexity of today? I believe is one of the greatest science fiction stories of all time!
ReplyDelete"Are you going to suggest the microbiologists who wrote this don't know what they are talking about and are blinded by their indoctrination into "Darwinism"?"
ReplyDeleteAre this microbioogist who suggested apes and humans benefit from higher level of mutations?
You understand the difference between the reproductive methods of bacteria and primates?
Do you have any idea of the generations during a "hard time" between bacterias and apes?
Darwinists have a problem when his histories are translated to the actual real world. That stories works only once upon a time far away.
Hi Computerist29,
ReplyDeleteThank you for providing your thoughts as to explanations of evolution.
You wrote...
"[Discrete differential evolution (DDE)] is completely anti-darwinian, in that changes do not correlate and are independent of random mutations and natural selection. They are discrete in that changes that occur can never be set back the same way an odometer can never be set back (unless its engineered or hacked otherwise). They are differential in that changes occur after a certain programmed condition is reached. Hence, they are restricted to the number of programmed conditions that can occur."
Would it be fair to summarize your explanations as "evolution events are preprogrammed triggers"?
How do you deal with short-term responses such as antibacterial resistance? Are you declaring them "microevolution" and not preprogrammed or are you suggesting they were preprogrammed too?
I don't want to go too far, too fast with my presumptions, so I will stop here. I look forward to reading your next comment.
Hi Blas,
ReplyDeleteYou wrote...
"Are this microbioogist who suggested apes and humans benefit from higher level of mutations?"
The names of the microbiologists are Armand Paauw, Maurine A. Leverstein-van Hall, Jan Verhoef, and Ad C. Fluit. If you are interested in finding out their position on ape/human link you might get lucky if you use Google Scholar.
"You understand the difference between the reproductive methods of bacteria and primates?
Do you have any idea of the generations during a "hard time" between bacterias and apes?
Darwinists have a problem when his histories are translated to the actual real world. That stories works only once upon a time far away."
As I understand it, most of the "hard time" was between bacteria and Precambrian animals like Vernanimalcula Quizhouena.
(see http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?act=ST;f=14;t=6612;st=30#entry166885)
The above link is to one of many comments I have posted arguing with ID critics that life is possibly "Front Loaded" to use Quantum Mechanics.
The Precambrian Vernanimalcula was too small (0.2mm) to be detected as a fossil until recently.
To me, this is evidence of a Fate' Compli. The Precambrian animals were already too complex and prewired to become an explosion of life's diversity on the planet Earth.
Evolutionary Biologists have compelling and detailed evidence tracing Bilateria animals, including Homo Sapiens and Vernanimalcula to common sources (for example, a lack of vitamin C biosynthesis in humans, monkeys and apes).
All of this could very well be God's plan. Bilateria could be a biblical "Kind".
Evolutionary Biologists are following the evidence where it leads them.
Do you have a counter hypothesis you would like to propose?
My counterhipotesis is lack of vitamin C during hard times will produce fasting aging, lower fertility, more illnes and if encrease the rate of mutation will reduce the population with big chances of extintion of the specie. I´m quite sure this hipotesis is more logic that the alternate. At least I do not heard anybody saying that the solution to the survival of apes in this hard times is irradiate them to encrease the rate of mutations.
ReplyDeleteHi Thought Provoker,
ReplyDelete"How do you deal with short-term responses such as antibacterial resistance? Are you declaring them "microevolution" and not preprogrammed or are you suggesting they were preprogrammed too?"
I would rid of "micro" and "macro" altogether. The primary difference is between adaptivity and non-adaptivity. Bacterial resistance is a form of adaptivity, I would say adaptivity is preprogrammed in the probabilistic sense: subset function AB(ABA) of set A (ie: A { AB(ABA) }), AB is dependent on set A, and ABA is dependent on AB, but ABA is independent of set A.
Hi Blas,
ReplyDeleteYou wrote...
"My counterhipotesis is lack of vitamin C during hard times will produce fasting aging, lower fertility, more illnes and if encrease the rate of mutation will reduce the population with big chances of extintion of the specie."
If you want to hypothesize a lack of vitamin C biosynthesis is nothing but bad news for humans, monkeys and apes, that is up to you. However, it isn't very supportive evidence for a benevolent designer of life.
Be it from random, quantum or divine sources and be it good or bad, the point is humans, monkeys and apes all have a lack of vitamin C biosynthesis due to a non-functioning L-gulonolactone oxidase gene; a gene which works fine for the bulk of mammals as well as some other animals.
Considing the evidence, one possibility is God fused the second and third gene of the Chimpanzee, along with some other minor adjustments, to create the human species. This wouldn’t be a difficult trick to accomplish through Quantum Effects.
I guess it is also possible God made it look like that is what he did, complete with maintaining the non-functioning L-gulonolactone oxidase gene in both Chimpanzees and humans. After all, who are we to question God’s mysterious ways?
Hi computerist29,
ReplyDeleteThank you for responding. I think I am understanding what you are saying, but let me ask two more probing questions. What is your take on Horizontal Gene Transfer (HGT)?
In a previous comment, I linked to a recent observation of HGT in a bacterial outbreak. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801613
But HGT also shows up at a larger scale in phylogenetic trees. http://www.biomedcentral.com/content/pdf/1471-2148-10-42.pdf
So is HGT form of adaptability in the “probabilistic sense”, or is it preprogrammed as a form of non-adaptivity in the set/sub-set sense, or both, or neither?
When you say “probabilistic sense” are you presuming randomness with a Gaussian distribution?
I tend to hold there is no such thing as randomness. So, in your terminology, everything is programmed. However, because of the inherent properties of Quantum Mechanics the programming is non-deterministic and so complex it appears random.
Quantum non-determinism approaches metaphysics. It could be random, it could be God, it could be anything we can imagine and even something we can’t.
"If you want to hypothesize a lack of vitamin C biosynthesis is nothing but bad news for humans, monkeys and apes, that is up to you. However, it isn't very supportive evidence for a benevolent designer of life"
ReplyDeleteWas I talking about a designer of life? Why bring this in?
"Be it from random, quantum or divine sources and be it good or bad, the point is humans, monkeys and apes all have a lack of vitamin C biosynthesis due to a non-functioning L-gulonolactone oxidase gene; a gene which works fine for the bulk of mammals as well as some other animals."
And so? Make this apes and humans better adapted to hard times? Do you find the logic that sees and advantage to lack the enzyme correct?