The biologically-based origin of the mammalian placenta (2)

The past is not the key to the present
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See also: The biologically-based origin of the mammalian placenta

I’ll preface this follow-up on the origins of the mammalian placenta with comments that attest to foolishness of theoretical physicists who try to link Big Bang cosmology to neo-Darwinian theories about mutations and evolution.

RPF Interviews Dr. Alexander Unzicker

Excerpt 1)  “It annoys me too much to see another generation of physicists deterred by the dumb messy patchwork called the standard model of particle physics, that hides the basic problems physics ought to deal with.”

My comment: It annoys me when evolutionary theorists make claims like this one: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” Mutation-Driven Evolution (p. 199)

Excerpt 2)  “This book won’t appeal to particle physicists there is no way to convince an expert that he or she has done nonsense for thirty years.”

My comment: My model does not appeal to physicists or to evolutionary theorists. Nutrient-dependent/pheromone-controlled adaptive evolution: a model eliminates the pseudoscientific nonsense about genomic conservation that somehow occurs outside the context of the biophysicallly constrained chemistry of protein folding via constraint-breaking mutation.

Clearly, however, I am not alone in my attempts to fight against the biologically uninformed physicists and extensions of their ridiculous theories to evolution via constraint-breaking mutation. The Law of Physics and Laws of Biology are not made to be broken by declarations that fail to mention the Laws. See for example the comments here:

Scientific method: Defend the integrity of physics

Excerpt: “…the issue boils down to clarifying one question: what potential observational or experimental evidence is there that would persuade you that the theory is wrong and lead you to abandoning it? If there is none, it is not a scientific theory.”

My comment: Experimental evidence of biologically-based cause and effect supports my model of cell type differentiation via amino acid substitutions, and my model refutes ideas about constraint-breaking mutations. In my model, mutations are constrained by RNA-mediated events linked to cell type differentiation, which explain why mutations do not lead to the evolution of anything in any species.

Genomic parasites (revisited)

See: Biologists link sexual selection and placenta formation (in fish)

Excerpt 1) “All placental mammals inherited their placenta from a single common ancestor that lived more than 100 million years ago,” he explained. “Whatever was happening then has long since been lost to history.”

My comment: That suggests whatever was happening in fish might be happening in mammals. Indeed, in a more recent news report, Victor Lynch claims to have found what was missing. “…we found the genetic changes that likely underlie the evolution of pregnancy are linked to domesticated transposable elements that invaded the genome in early mammals. So I guess we owe the evolution of pregnancy to what are effectively genomic parasites.”

What aspect of these genomic parasites explains their link to the evolution of pregnancy via links from a common ancestor? Was the common ancestor an egg-laying fish? If so, how are genomic parasites linked to sexual selection and placenta formation in fish?

Excerpt 2 from Biologists link sexual selection and placenta formation) “Describing the life histories of more than 150 species of fish in the family Poeciliidae, the researchers found that species with placentas tend to have males that do not have bright coloration, ornamentation or courtship displays. They tend to be much smaller than the males of species without placentas. They also tend to be very well endowed, enabling males to sneak up on females to mate with them without the formality of courtship.”

My comment: Did genomic parasites cause all of those differences; some of them — any of them? Where’s the experimental evidence? Remember what Ellis and Silk (2014) said: “If there is none, it is not a scientific theory.”

Where did these genomic parasites come from? John Sedivy seems to be suggesting in this video (see 11:38 – 11:54) that the genomic parasites are “…molecular parasites that date back to the prebiotic dawn of time” (e.g., at the time when RNA was the first self-replicating molecule). See: Chromatin and epigenetic dynamics in senescence phenotypes – John Sedivy

That makes sense if the function of nutrient-dependent changes in the microRNA/messenger RNA balance link control of the DNA damage that transposons cause, via RNA-directed DNA methylation and RNA-mediated amino acid substitutions that link the pheromone-controlled physiology of reproduction to biodiversity in species from microbes to man. However, if the amino acid substitutions also lead to nutrient-dependent pheromone-controlled ecological adaptations, the theories of physicists and evolutionists are nothing more than pseudoscientific nonsense, which is what creationists believe.

If there is no scientific theory to support what you believe, the problem may be that you are a physicist or evolutionist. If what you observe about the obvious complexity of biodiversity is akin to what Darwin observed when he proposed that ‘conditions of life’ must be considered before natural selection or sexual selection are relevant, you may be a creationist, like Dobzhasky, who wrote: “…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.” — in  Nothing in Biology Makes Any Sense Except in the Light of Evolution

If he were not still dead, I’m rather certain he would by now have realized that amino acid substitutions differentiate all cells of all individuals of all species and mutations cause physiopathology. See also: Combating Evolution to Fight Disease. Unfortunately, others still don’t know the difference between an amino acid substitution and a mutation. See, for example:

In a New Approach to Fighting Disease, Helpful Genetic Mutations Are Sought

Excerpt: “After years of looking for mutations that cause diseases, investigators are now searching for those that prevent them.”

My comment: Mutations cause diseases, fixed amino acid substitutions prevent them. See instead:

A recurrent regulatory change underlying altered expression and Wnt response of the stickleback armor plates gene EDA

Excerpt: “This regulatory change thus alters EDA expression at the same body site where freshwater fish lack body armor, while preserving important functions of EDA in other tissues. These results provide a new example of a specific regulatory change linked to morphological evolution in natural populations (Martin and Orgogozo 2013), and  add to growing evidence that regulatory changes are a predominant mechanism underlying adaptive evolution in sticklebacks (Jones et al. 2012) and other organisms (Wray 2007, Carroll 2008).”

My comment: A mutation links the lack of body armor in fish from the FGFR3 to more than 99 percent of cases of human achondroplasia, which is a form of short-limbed dwarfism. “Specifically, the protein building block (amino acid) glycine is replaced with the amino acid arginine at protein position 380 (written as Gly380Arg or G380R). Researchers believe that this genetic change causes the receptor to be overly active, which leads to the disturbances in bone growth that occur in this disorder.” FGFR3

Mutated FGFR3 genes also are linked to a variety of other diseases and disorders. “Among 62 human cases of seborrheic keratosis (182000), Logie et al. (2005) found that 39% of samples harbored somatic activating FGFR3 mutations, identical to those associated with skeletal dysplasia syndromes and bladder and cervical neoplasms (see, e.g., 134934.0005 and 134934.0013). Logie et al. (2005) implicated FGFR3 activation as a major cause of benign epidermal tumors in humans.” FIBROBLAST GROWTH FACTOR RECEPTOR 3; FGFR3

Why haven’t others learned the difference between fixed amino acid substitutions that stabilize the DNA in organized genomes and mutations? The answer to that question takes us back to what’s known about physics. For example, extended discussion of Atoms can be in two places at the same time led to this claim:

I wrote: “Mutagenesis experiments take meaningless results and meaningfully interpret them. Most people are intelligent enough to know that — even if they are, like you, biologically uninformed.

Andrew Jones responded with a link to a 2001 publication: How so? The basic idea of them is introducing random changes to enzymes and observing their effects.

Mutagenesis (link opens pdf)They bring it up in that paper and I’ve brought it up before- if mutations can never be beneficial, then the SOS response wouldn’t exist.

My comment: He linked to a 2001 paper that claims: “…the increased expression of a number of genes whose products not only assist the cell to survive DNA damage but also increase mutation rates (Friedberg et al., 1995; Frank et al., 1996, and see below).”

Our 1996 review Hormones and Behavior review links RNA-mediated cell type differentiation from species of microbes to man via the conserved molecular mechanisms of what is now known to be the biophysically constrained chemistry of protein folding by amino acid substitutions, which is what I detailed in my 2013 review with examples of cause and effect across species. Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Andrew Jones is more than a decade behind the experimental evidence I used to support my model.

See also:

Diet and nutrition essential for mental health

“…many of these nutrients have a clear link to brain health, including omega-3s, B vitamins (particularly folate and B12), choline, iron, zinc, magnesium, S-adenosyl methionine (SAMe), vitamin D, and amino acids.”

What’s not clear is how researchers can continue to ignore the obvious fact that nutrient-dependent RNA-directed DNA methylation links RNA-mediated events from quantum physics to quantum biology and behavior via amino acid substitutions that differentiate the cell types of all cells in all individuals of all species during their development.

See for example: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults

Again, see my model: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. There is no excuse for anyone willing to learn to not realize that “If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based.” (p. 1014) — Neo-Darwinism, the Modern Synthesis and selfish genes: are they of use in physiology?

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