Neofunctionalization as evidence for evolution now debunked

Neofunctionalization is based on epigenetic reprogramming

During last two decades, so called neofunctionalization was thought to be an evolutionary process by which a cell generates random gene duplications and these duplications are mutated and in this way, organisms could produce new functions or even structures. Very often neofunctionalization has been a strong argument for evolution believers. Today modern science proves these claims wrong.

https://advances.sciencemag.org/content/5/7/eaaw7006

"Furthermore, sex change involves distinct epigenetic reprogramming and an intermediate state with altered epigenetic machinery expression akin to the early developmental cells of mammals."

"Together, this indicates that like H3K27 modification, there is an intense period of DNA methylation reprogramming in the gonad at intermediate stages of sex change. Such distinct sex-specific expression of DNA methyltransferase genes and other epigenetic modifiers was also recently observed in gonadal transcriptomes of other sex-changing fishes and may be important for sexual plasticity."

"Transcriptomic and methylome analyses across sex change in the iconic bluehead wrasse have identified the triggers of socially induced sex change and enactors of gonadal metamorphosis. Our results suggest that the environmental stimulus is exerted via stress, that the subsequent steps involve repression of aromatase, and that distinctive epigenetic reprogramming is associated with reengineering ovaries into testes. Importantly, this does not occur by direct transdifferentiation but involves an intermediate state with altered epigenetic machinery expression that is reminiscent of mammalian naïve pluripotent stem cells and PGCs."

"Gene neofunctionalization following duplication allows for diversification of a standard genetic network and may be one factor contributing to the sexual plasticity that is characteristic of fishes."
 

"The use of neofunctionalized paralogs in sex change was not restricted to hormonal and signaling pathways; we also found duplicated epigenetic machinery in bluehead wrasses that exhibited female- or male-specific expression. Global DNA methylation was remodeled, as expression of female-specific DNMTs was replaced with male-specific expression. The peak in TET expression seen at this time indicates remodeling of DNA methylation that is typical of mammalian PGCs and both naïve and classically grown pluripotent stem cells. The same appeared to be true for histone-modifying machinery; the PRC2 complex is associated with differentiation in mammals and showed high expression in cells belonging to committed sexual phenotypes but was deactivated in the gonads of transitional fish. Likewise, dynamic expression of histone demethylases, acetyltransferases, and variant histones further suggest active chromatin modification during gonadal sex change."

Summary: 

• Stress factors, such as diet type or sex ratios trigger epigenetic modifications.
• Gene duplications in these adaptive processes are based on epigenetic mechanisms and factors.
• The cell is able to modify a novel gene in order to achieve adaptational purposes.
• Organismal change is based on complex epigenetic mechanisms and especially epigenetic reprogramming.
• In this process DNA is just passive information and it has no control over cellular processes.

Highly optimized and polyfunctional DNA code doesn't tolerate mutations

Random mutations never result in any kind of evolution

https://www.worldscientific.com/doi/epdf/10.1142/9789814508728_0006

Excerpts: "There is growing evidence that much of the DNA in higher genomes is poly-functional, with the same nucleotide contributing to more than one type of code. Such poly-functional DNA should logically be multiply-constrained in terms of the probability of sequence improvement via random mutation. We describe a model of this relationship, which relates the degree of poly-functionality and the degree of constraint on mutational improvement. We show that: a) the probability of beneficial mutation is inversely related to the degree that a sequence is already optimized for a given code; b) the probability of beneficial mutation drastically diminishes as the number of overlapping codes increases. The growing evidence for a high degree of optimization in biological systems, and the growing evidence for multiple levels of poly-functionality within DNA, both suggest that mutations that are unambiguously beneficial must be especially rare. The theoretical scarcity of beneficial mutations is compounded by the fact that most of the beneficial mutations that do arise should confer extremely small increments of improvement in terms of total biological function. This makes such mutations invisible to natural selection. Beneficial mutations that are below a population's selection threshold are effectively neutral in terms of selection, and so should be entirely unproductive from an evolutionary perspective. We conclude that beneficial mutations that are unambiguous (not deleterious at any level), and useful (subject to natural selection), should be extremely rare."

"To further test the effect of multiple constraints on the appearance of beneficial mutations, we constructed a simple poly-constrained artificial system based on English crossword puzzles. Crossword puzzles, for our purpose, are simply collections of words with overlapping, shared letters among some of the words. Figure 6 [the picture below] contains an illustration of such puzzles. We are most familiar with two- dimensional crossword puzzles, where up to two words may share a single letter, but crossword puzzles can be extended to many dimensions. An L-dimensional crossword puzzle is here defined as a collection of words, such that up to L words may share a single, overlapping letter, for one or more letters in the puzzle. Each overlap forms a constraint on our puzzle, which limits the possible letters that are allowed in a given position. Increasing the number of words that share a single letter increases the number of constraints on that particular letter, and limits the number of values that letter position may take."

Crossword puzzles are familiar poly-constrained systems. Intersecting words create constraints on overlapping letters, such as the E of FILE in the first puzzle. Although a viable, functional mutation may change FILE to FILL, this would simultaneously change INTOLERANT to the non-functional INTOLLRANT, a non-word. As we increase the number of dimensions, the number of overlapping words can increase as well, further preventing beneficial changes.

My comment: DNA reading mechanisms are able to read DNA from different locations and in both directions (3' and 5'). Words being read often overlap with each other and very often words are palindromes. Especially human genome is so perfectly organized and optimized that it doesn't tolerate random mistakes. This is why there are no fully beneficial mutations in human genome. Instead, the number of harmful genetic errors will soon exceed 2 million at population level. Evolution never happened. Don't be deceived.

Identical genes but non-identical phenotypes

DNA doesn't determine phenotype or organismal traits

1. At cellular level

https://medcraveonline.com/MOJCSR/epigenetic-regulation-mechanisms-in-stem-cell-differentiation.html
 

Excerpt: "Stem cells give rise to almost 200 different cell types that are present in a mammalian organism. In spite of the fact that these distinct cell types have different functions and morphologies, they descend from a common ancestor cell and essentially share the same DNA. The underlying cause for the rise of specific cell types is not genetic differences; it is mostly due to how the genetic information is interpreted. The epigenome, which consists of several degrees of regulatory mechanisms, dictates the gene expression profile of a certain type of cell. Eukaryotic DNA is packaged into chromatin, folded and compacted which in turn affects its functionality as certain regions of DNA will not be accessible whereas some other regions will be easier to access for effect or proteins and modifiers to bind. The chromatin dynamics are modulated by several machineries including but not limited to histone PTMs and their variants, DNA methylation and RNA interference, which have crucial roles in regulating stem cell differentiation, cell fate determination and lineage specification."

2. At tissue level

https://www.colorado.edu/today/2020/07/07/how-does-stem-cell-know-what-become-study-shows-rna-plays-key-role

Excerpts: "Look deep inside our cells, and you’ll find that each has an identical genome –a complete set of genes that provides the instructions for our cells’ form and function.

But if each blueprint is identical, why does an eye cell look and act differently than a skin cell or brain cell? How does a stem cell – the raw material with which our organ and tissue cells are made – know what to become?
 

“All genes are not expressed all the time in all cells. Instead, each tissue type has its own epigenetic program that determines which genes get turned on or off at any moment,” said co-senior author Thomas Cech, a Nobel laureate and distinguished professor of biochemistry. “We determined in great detail that RNA is a master regulator of this epigenetic silencing and that in the absence of RNA, this system cannot work. It is critical for life.”"

3. At body plan level

https://ussromantics.com/2020/01/03/epigenetics-and-imprinting-2-identical-genes-and-non-identical-phenotypes/

Excerpt: "it’s obvious that genetics isn’t the whole story of our inheritance and development because it doesn’t begin to explain how, from one fertilised egg – the union of, or pairing of, two sets of chromosomes – we get, via divisions upon divisions upon divisions, a complex being with brain cells, blood cells, skin cells, liver cells and so forth, all with identical DNA. It also doesn’t explain how a maggot becomes a fly with the same set of genes (or a caterpillar becomes a butterfly, to be a little more uplifting). These transformations, which maintain genetic inheritance while involving massive change, must be instigated and shaped by something over and above genetics but intimately related to it – hence epigenetics. Other examples include whether a crocodile hatchling will turn out male or female – determined epigenetically via the temperature during development, rather than genetically via the Y chromosome in mammals.
 

So, to add to the description I gave last time, the histone proteins that the DNA wraps itself round come in batches or clusters of eight. The DNA wraps around one cluster, then another, and so on with millions of these histone clusters (which have much-studied ‘tails’ sticking out of them). And I should also remind myself that our DNA comes in a four-letter code strung together, out of which is constructed 3 billion or so letters."

My comment: With the same set of DNA there could be a huge number of different phenotypes or outcomes. DNA doesn't determine phenotype or organismal traits or characteristics. It's all epigenetics. DNA does nothing without epigenetic programming. In other words, without epigenetic information profiles the DNA is just passive information.