It might be amusing if the misrepresentations of links between energy and cell type differentiation by people like PZ Myers were not going to cause more suffering and death.  Instead, two years after his attack on me for my accurate representations of the link from nutrient energy-dependent chromosomal rearrangements to pheromone-controlled biodiversity in species from microbes to humans we see this:

You’re trying to explain a random phenotype by looking for a randomization mechanism in the genome.

No one will ever try to do that again. Barbara McClintock’s Nobel Prize-winning works showed that morphological and behavioral phenotypes are RNA-mediated before anyone knew anything about DNA repair. Like others, she was not trying to explain randomness, she used experimental evidence of biologically-based cause and effect, which is what is required to win the Nobel Prize in Physiology or Medicine.

Serious scientists cannot just invent theories based on their assumptions about random events. Even though Barbara McClintock did not know the molecular mechanisms of RNA-mediated DNA repair, she showed that random mutations were not the source of increasing organismal complexity.

Perry Marshall, author of Evolution 2.0: Breaking the Deadlock Between Darwin and Design tried to explain to PZ Myers how a pattern of nutrient-dependent RNA-mediated DNA repair is linked to all biodiversity. Myers doesn’t like Marshall’s non-technical semi-biological engineering approach to information-driven biologically-based cause and effect.

Myers doesn’t like any approach that challenges his ridiculous assumptions.

See also: Feedback loops link odor and pheromone signaling with reproduction, which was co-authored by 2004 Nobel Laureate Linda Buck, who shared the Prize in Physiology or Medicine with Richard Axel.

See also: Life, logic and information by 2001 Nobel Laureate, Sir Paul Nurse.


Pulses of information sent along the telegraph generate a code for letters and as a consequence sentences can be communicated. This converts the same signalling pathway from a simple on/off switch to a device that can transfer, for example, the works of Shakespeare. (p. 426) It is likely that dynamics has been exploited more generally in the evolution of biological systems for signalling purposes, allowing the communication of more complex information.

Note, however, that he also claims

Living machines are not intelligently designed and will often be redundant and overly complex.

PZ Myers accepts the second statement, but not the first. What’s more annoying than PZ’s misrepresentations of some or all of the Nobel Prize winning works from 1983 to 2015 in Physiology or Medicine, is that Myers still cannot grasp the fact that mutations are linked to pathology, not to ecological adaptations.

Without ecological adaptations there is no biodiversity. Accumulated mutations are linked to information loss and the undifferentiated cell types of cancer, not to the evolution of one species from another.

Ecological variation must lead to ecological adaptations, and the only pathway that links variation to adaptation is RNA-mediated DNA repair. All serious scientists know this. They might disagree with the beliefs of other serious scientists but all must link nutrient energy-dependent base pair substitutions from changes in the microRNA/messenger RNA balance to RNA-mediated cell type differentiation.

Adhesion proteins link feedback loops to link fixation of amino acid substitutions in histones. Fixation links supercoiled DNA in the organized genomes of all living genera to protection against virus-driven entropy. The proliferation of viruses links viral microRNAs to perturbed RNA-mediated protein folding, called mutations, and to all pathology.


1) Elucidating MicroRNA Regulatory Networks Using Transcriptional, Post-transcriptional, and Histone Modification Measurements

2) Structural diversity of supercoiled DNA

3) Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity

4) The octopus genome and the evolution of cephalopod neural and morphological novelties

5) Role of olfaction in Octopus vulgaris reproduction


Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000). — p. 61

These authors cited two works that link RNA-mediated cell type differentiation to behavior. One, in insects Organizational and activational effects of hormones on insect behavior.

The other is also linked to a model of RNA-mediated cell type differentiation in species from microbes to humans.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

In the context of links from all invertebrates to all vertebrates via conserved molecular mechanisms, what does PZ Myers hope to prove to anyone about mutations and evolution, or about his level of ignorance?

See also: Electrical Fields Guiding 3D Shape of Cells and Organs


…modern science cannot calculate what shape a 400 amino acid coded sequence will be when it folds into a protein. It would take all the supercomputers together two thousand years to calculate the folding of one average protein. Yet, proteins assemble into the exact shape in a millisecond, helped by very complex chaperone molecules. Cells routinely edit their messenger RNA with alternative splicing to make a whole variety of shapes.

My comment: The structure and function of those shapes links the nutrient-dependent pheromone-controlled RNA-mediated cell type differentiation of species from microbes to humans via fixation of amino acid substitutions in the histones of supercoiled DNA.

See also: The majority of transcripts in the squid nervous system are extensively recoded by A-to-I RNA editing


…highly edited sites within conserved domains tend to recode to amino acids that occur frequently in other species at the same position (Figure 4–figure supplement 3), suggesting selection towards functional substitutions and against deleterious ones.

My comment: There is not one hint in the experimental evidence published by serious scientists that selection is random. If there were, people like PZ Myers would cite sources that support their ridiculous claims.

See for comparison: Origins of De Novo Genes in Human and Chimpanzee


Our results indicate that the expression of new loci in the genome takes place at a very high rate and is probably mediated by random mutations that generate new active promoters. These newly expressed transcripts would form the substrate for the evolution of new genes with novel functions.

See for a refutation of that neo-Darwinian nonsense: Nothing in Biology Makes Any Sense Except in the Light of Evolution (p. 127)


For example, the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.

See also: Large Numbers of Novel miRNAs Originate from DNA Transposons and Are Coincident with a Large Species Radiation in Bats


In an effort to be conservative in our language and to distinguish between experimentally validated or known miRNAs and those identified here, based on our expression and computational predictions, we prefer to refer to the latter by a term other than miRNA. The term milRNA (miRNA-like) is already used to refer to a class of small RNAs in fungi that are generated by a distinct biological pathway (Kang et al. 2013; Lau et al. 2013). We will therefore refer to our proposed putative miRNAs as p/miRNAs.

My comment: I was not surprised to see David Ray, the principle investigator from this group try to support the claims of PZ Myers. David’s group is also trying to remove consideration for the role of nutrient energy-dependent microRNAs. He uses a mathematical model, a definition, and assumptions like all other pseudoscientists have done.

Putative miRNAs or p/miRNAs are like de novo genes. When pseudoscientists don’t know where they come from, they claim the automagically appeared or emerged at precisely the time they needed them to support their ridiculous theories.  Then, they use their ridiculous theories to dismiss the claims about “conditions of life” made by everyone from Darwin to Di Cosmo.

See also: Habitat variability does not generally promote metabolic network modularity in flies and mammals


…the frequency of gene duplication appears to be the main factor contributing to network modularity. These findings raise the question of whether or not there is a general mechanism for habitat range expansion at a higher level (i.e., above the gene scale).

My comment: I’m not going to request any more reprints from people who appear to be supporters of neo-Darwinian nonsense. Gene duplication is nutrient-dependent and it is controlled by the physiology of reproduction in all living genera. The links from the epigenetic landscape to the physical landscape of supercoiled DNA have confirmed everything any serious scientist thought about cell type differentiation. There is no defined limit between epigenetics and genetics, and there is no definition that can be used by theorists to separate nutrient-dependent metabolic networks from genetic networks.


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