Natural Selection Not The Only Process That Drives Evolution?

[mercurial]

ScienceDaily (Jan. 28, 2009) — Why have some of our genes evolved rapidly? It is widely believed that Darwinian natural selection is responsible, but research led by a group at Uppsala University, suggests that a separate neutral (nonadaptive) process has made a significant contribution to human evolution.

Their results have been published January 27 in the journal PLoS Biology.

The researchers identified fast evolving human genes by comparing our genome with those of other primates. However, surprisingly, the patterns of molecular evolution in many of the genes they found did not contain signals of natural selection. Instead, their evidence suggests that a separate process known as BGC (biased gene conversion) has speeded up the rate of evolution in certain genes. This process increases the rate at which certain mutations spread through a population, regardless of whether they are beneficial or harmful.

"The research not only increases our understanding of human evolution, but also suggests that many techniques used by evolutionary biologists to detect selection may be flawed," says Matthew Webster of the Department of Medical Biochemistry and Microbiology at Uppsala University.

BGC is thought to be strongest in regions of high recombination, and can cause harmful mutations can spread through populations. The results lead to the provocative hypothesis that, rather than being the result of Darwinian selection for new adaptations, many of the genetic changes leading to human-specific characters may be the result of the fixation of harmful mutations. This contrasts the traditional Darwinistic view that they are the result of natural selection in favour of adaptive mutations.

Link

 

[Phronesis]

From the article:
Hotspots of Biased Nucleotide Substitutions in Human Genes

Genes that have experienced accelerated evolutionary rates on the human lineage during recent evolution are candidates for involvement in human-specific adaptations. To determine the forces that cause increased evolutionary rates in certain genes, we analyzed alignments of 10,238 human genes to their orthologues in chimpanzee and macaque. Using a likelihood ratio test, we identified protein-coding sequences with an accelerated rate of base substitutions along the human lineage. Exons evolving at a fast rate in humans have a significant tendency to contain clusters of AT-to-GC (weak-to-strong) biased substitutions. This pattern is also observed in noncoding sequence flanking rapidly evolving exons. Accelerated exons occur in regions with elevated male recombination rates and exhibit an excess of nonsynonymous substitutions relative to the genomic average. We next analyzed genes with significantly elevated ratios of nonsynonymous to synonymous rates of base substitution (dN/dS) along the human lineage, and those with an excess of amino acid replacement substitutions relative to human polymorphism. These genes also show evidence of clusters of weak-to-strong biased substitutions. These findings indicate that a recombination-associated process, such as biased gene conversion (BGC), is driving fixation of GC alleles in the human genome. This process can lead to accelerated evolution in coding sequences and excess amino acid replacement substitutions, thereby generating significant results for tests of positive selection.

Conclusion:

We have presented evidence that protein-coding sequences with accelerated rates of evolution in humans have significantly biased patterns of nucleotide substitutions. These results are consistent with a strong effect of W→S fixation bias on the evolution of the most rapidly evolving coding exons in our genome. This process may have led to the increased fixation of replacement amino acid changes on the human lineage, and may bias tests of positive selection.

Well, will you look at that. Biased patterns of nucleotide substitutions. Now concider the following:
An End to Endless Forms: Epistasis, Phenotype Distribution Bias, and Nonuniform Evolution

These findings complement the view of development as a key component in the production of endless forms and highlight the crucial role of development in constraining biotic diversity and evolutionary trajectories.

The role of development in generating, or constraining, biotic diversity has been one of the most active debates in evolutionary biology [32]–[34]. The roots of this debate go back to the study of homologies and questions over physico-chemical verses genetically-selected rules of growth. One merit of simple developmental models is to illustrate how these two positions reflect necessary, complementary properties of generic developmental programs. Regulatory epistasis introduces non-linearities into development, allowing similar genotypes to generate significant divergence among phenotypes, whereas degeneracy tends to contract the occupancy of morphospace and bias phenotypic samples. Of great interest is how these structural properties of development have themselves been modified over the course of evolutionary time, potentially changing the tempo and mode of the evolutionary process. One of the paradoxical implications of this study has been to show how innovations in development (arising through increasing regulatory dimensions) that lead to an increase in the volume of accessible phenotypes, can lead to a reduction in selective variance (through increasing regulatory epistasis), so whereas the potential for novel phenotypes increases, the fraction of space these phenotypes occupies tends to contract. Hence the evolutionary process moves from a macro-configuration, sampling distant regions of space sparsely, to a micro configuration, sampling local regions of space at high resolution. This is analogous to an annealing process, whereby as an optimization process proceeds, the solutions become more frequent and more densely localized around the putative solution points.

• Evolution is constrained as a result of genetic information present in simpler genetic controls dating from the base of the evolutionary tree (preadaptations)..
• We observe many preadaptations for multicellularity in primitive unicellular organisms.
• Also several toolkits (also preadaptations) for the development of body plans (Hox genes), the nervous system and sensory organs in animals at the base of the eumetazoan tree.
• Also, spectacular examples of convergence are observed in nature.

As seen in the evolution of eyes, as soon as these sets of genes were formed (E.g. Pax genes), through whatever mechanism), evolution seemed to have been biased to a few end points, and these few endpoints arose 40-60 times, independently, as a result of pre-existing (preadaptations) information in the case of eyes.

What other "biased" end points can there be? Nervous systems, smell, hearing?

Why would evolution be biased, as in development, to only reach a few end points over and over?

Natural selection as an explanation for variety can now safely be relegated as a secondary force, with cellular mechanisms showing an increasing importance in biasing evolutionary trajectories.

 

[BCO]

From the article:
Hotspots of Biased Nucleotide Substitutions in Human Genes


Conclusion:


Well, will you look at that. Biased patterns of nucleotide substitutions. Now concider the following:
An End to Endless Forms: Epistasis, Phenotype Distribution Bias, and Nonuniform Evolution

• Evolution is constrained as a result of genetic information present in simpler genetic controls dating from the base of the evolutionary tree (preadaptations)..
• We observe many preadaptations for multicellularity in primitive unicellular organisms.
• Also several toolkits (also preadaptations) for the development of body plans (Hox genes), the nervous system and sensory organs in animals at the base of the eumetazoan tree.
• Also, spectacular examples of convergence are observed in nature.

As seen in the evolution of eyes, as soon as these sets of genes were formed (E.g. Pax genes), through whatever mechanism), evolution seemed to have been biased to a few end points, and these few endpoints arose 40-60 times, independently, as a result of pre-existing (preadaptations) information in the case of eyes.

What other "biased" end points can there be? Nervous systems, smell, hearing?

Why would evolution be biased, as in development, to only reach a few end points over and over?

Natural selection as an explanation for variety can now safely be relegated as a secondary force, with cellular mechanisms showing an increasing importance in biasing evolutionary trajectories.

tldr

 

[Phronesis]

The title of the article is misleading. Natural selection does not drive ANYTHING. It does nothing. As so well put by Will Provine in his book:
The Origins of Theoretical Population Genetics
From page 199 (see above link):

As John Endler has argued eloquently in Natural Selection in The Wild (1968), natural selection is not a mechanism. Natural selection does not act on anything, nor does it select (for or against), force, maximize, create, modify, shape, operate, drive, favor, maintain, push or adjust. Natural selection does nothing. Natural selection as a natural force belongs in the insubstantial category already populated by the Becker/Stahl phlogiston (Endler 1986) or Newton's "ether".
Natural selection is the necessary outcome of discernible and often quantifiable causes.

Natural selection DOES NOTHING. The true agents of change are cellular mechanisms. Mechanism, mechanisms, mechanisms, all wrapped up in a near universal and superbly optimal genetic code (wait for the discoveries on the epigenetic code) driven by biomolecular machines, quality control programs and variation inducers. Nano-intentional entities capable of manipulating information and biasing evolutionary trajectories.

 

[hellhound604]

lol ..... debate continues .....

as well as Natural Selection, there are Kin Selection and Sexual selection that all drives species into new directions ....