#72. Why There is Sex [evolution]

EV

Red, theory; black, fact.

The flower Coronilla varia L.

Sex is an evolvability adaptation

There are always two games in town: reproduction and evolution. Since we live on an unstable planet where the environment can change capriciously, species here have been selected for rapid evolvability per se to enable them to adapt to the occasional rapid environment changes and not go extinct. Apparently, mutations, the starting point for evolutionary adaptation, become more common when the organism is stressed, and stress may partly be a forecast of loss of fertility due to a developing genome-environment mismatch. Bacteria exhibit the large mutation of transformation under stress conditions, and 3 types of stress all increased the meiotic recombination rate of fruit flies (Stress-induced recombination and the mechanism of evolvability. Zhong W, Priest NK. Behavioral ecology and sociobiology. 2011;65:493-502). Recombination can involve unequal crossing-over in which changes in gene dose can occur due to gene duplication or deletion. However, since most mutations are deleterious (there are more ways to do something wrong than to do it better) many mutations will also reduce fertility, and at precisely the wrong moment: when a reduction in fertility is impending due to environment change. The answer was to split the population into two halves: the reproduction specialists and the selection specialists, and remix their respective genomes at each generation.

The roles of the two sexes

Females obviously do the heavy lifting of reproduction, and males seem to be the gene testers. So if a guy gets a bad gene, he dies, ha ha, and the luckier guy next to him then gets two wives. The phenomenon of greater male variability (Greater male than female variability in regional brain structure across the lifespan. Wierenga LM, Doucet GE, Dima D, Agartz I, Aghajani M, Akudjedu TN, Albajes‐Eizagirre A, Alnæs D, Alpert KI, Andreassen OA, Anticevic A. Karolinska Schizophrenia Project (KaSP) Consortium. Hum. Brain Mapp., doi. 2020;10, and I have never seen so many authors on a paper: 160.) suggests that mutations have more penetrance in males, as befits the male role of cannon fodder/selectees. What the male brings to the marriage bed, then, is field-tested genetic information. Male promiscuity can therefore be seen as a necessary part of this system, which allows many mutations to be field tested with minimal loss of whole-population fertility, because it is the females who are the limiting factor in population fertility.

Chromosomal mechanisms of greater male variability

Chromosomal diploidy may be a system for sheltering females from mutations, assuming that the default process is for the phenotype that develops to be the average of the phenotypes individually specified by the paternal and maternal chromosome sets. Averaging tends to mute the extremes. The males, however, may set up a winner-take-all competition between homologous chromosomes early in development, with inactivation of one of them chosen at random. The molecular machinery for this may be similar to that of random x-inactivation in females. The result will be greater penetrance of mutations through to the phenotype and thus greater male variability. 

Quantitative prediction

This reasoning predicts that on a given trait, male variability (as standard deviation) will be 41% greater than the female variability, a testable prediction. 41% = [SQRT(2) -1] × 100. Already in my reading I have found a figure of 30%, which is suggestive. 

Now all I have to do is reconcile all this with the laws of Mendelian inheritance. 

Mechanistic reconciliation with Mendel's laws

09-16-2021: This reconciliation seems to require an exemption mechanism built into the postulated chromosome inactivation process that operates on genes present in only one copy per parent. The effect of this mechanism will be to double the penetrance of dominant alleles at that gene. Therefore, in males, at single-copy genes, evolution of the machinery of sex is driven by the favorable mutations.

A lovers' heart drawn in dust

#60. Gender is Pecking Order [evolutionary psychology]

EP

Red, theory; black, fact.

Gender is pecking order

Gender, social status, and testosterone are clearly interrelated, but exactly how requires clarification when the very nature of gender is in question, as now. One possibility is that the male pecking order sits directly atop the female pecking order, and there is no barrier between. Thus, a male who falls low enough in the male pecking order will undergo a reversal in gender identification from male to female (and maybe keep on going down) and a female who rises high enough in the female pecking order will likewise undergo a reversal in gender identification from female to male (and maybe keep on going up). The entire structure could be called "the" pecking order, with the statistical median of the status ranks, and possibly the ranked testosterone levels, always dividing females from males, at least in terms of gendered social signaling. This could be an example of what is called an exact theory replacing its approximate counterpart. In this case, the corresponding approximate theory would be the gender binary. ("You are either a man or a woman.")

Recent history of trans

Since the early sixties, we have seen a trend of increasing media exposure of trans and non-binary individuals, and this was also a period of ever-increasing human population numbers. I conjecture that the latter trend caused the former. The population trend may have produced an upward trend in the average population density at which people are living, suburban expansion notwithstanding. This may have caused an increasing incidence of aggressive one-on-one interactions among humans due to the Calhoun effect, which is much discussed in these pages. (See post #37.) Aggressive, one-on-one interactions are well known to change the social status of the combatants, the winner enjoying increased status (i.e., a higher ranking in the pecking order) and the loser suffering reduced status. Overall, population density increases can thus be expected to increase the amount of traffic on the social ladder, both upward and downward, leading to increasing numbers of individuals crossing the median and becoming trans or nonbinary. The increasing numbers of trans and nonbinary individuals in society was then faithfully reflected in the content of the news stories of the day. QED.

Trans and development

By the status-is-gender theory, the occurrence of trans and binary individuals should run in families, since a large part of social status is hereditary, although it is not necessarily determined directly by the genome. Status may be influenced by multimodal acquisition of a status "calibration" from caregivers early in life that is synaptically mediated yet resistant to change after a critical period is past. A similar and well established phenomenon would be the early maladaptive schema, and this may amount to the same thing by a different name if status defaults to maximal at birth and is then adaptively reduced by experience.

Trans not genetically determined

Consistent with this, PLOS blogger R. Lewis, who has a PhD in genetics, found remarkably little evidence of a direct genetic causation in transgenderism. Moreover, out of 58 studies on "transgender" listed on clinicaltrials.gov, nothing worth mentioning was found about genetics. This could be an instance of the filing-drawer effect (negative results not published but left to languish in the filing cabinet).

Tangent: how pecking-order dynamics may lead to dispersal

02-29-2020: I am indebted to Jordan Peterson for turning me on to the pecking-order idea. It can explain aspects of dispersalism, as follows: If people have no emotional memory of their social wins and losses, we would expect their distribution on the social ladder to be Gaussian (aka, a bell curve). However, if a win or loss leaves you with an emotional residue of optimism or pessimism (and, of course, it does), a positive feedback can set in if conflicts are coming faster than the emotional fallout from each can dissipate, so that the more you lose, the greater your pessimism, and the more likely you are to lose in the future. Moreover, the more you win, the greater your optimism, and the more likely you are to win in the future. <08-29-2020: Following Peterson, this emotional fallout effect may be due to prolonged up- and down-regulations of serotonin concentrations in the brain.> This dynamic then splits the population into a bi-modal social distribution of oppressors and oppressed, and the latter soon join some refugee stream, resulting in dispersal. The frequency of conflicts could be measuring population density, and the conflicts would not necessarily be over resources, but over proxies for these such as land or jobs. With the addition of these ideas, the splitting and separation of overcrowded rodent populations in the behavioral-sink phase of a Calhoun experiment is explained. To connect these ideas with my earlier idea of the sadness cycle, I conjecture that sadness and its attendant social signaling expresses anger colored by pessimism about winning, whereas contempt and its social signaling expresses anger colored by optimism about winning.

A false-flag strategy?

20-08-2020: Another idea about trans is that it is a false-flag strategy used by low-status males and females to reproduce without punishment. Pair a gay woman with a trans woman and you have a potentially fertile couple able to fool the oppressors until the deed is done. Likewise a gay man and a trans man.

Photo by Jonny Gios on Unsplash

#39. Can Irreducible Complexity Evolve? [genetics, evolution]

EV     GE     

Red, theory; black, fact.

5-26-2018: Influential biologist Richard Dawkins wrote in "The God Delusion" that a genuine case of irreducible complexity will never be found in biology. A case of irreducible complexity would be some adaptation that would require an intelligent designer because it could never evolve one mutation at a time, and Dawkins believes there is no such intelligent designer in biology.

In classic natural selection, each mutation must be individually beneficial to its possessor in order for selection to increase its prevalence in the population to the point where the next incremental, one-mutation improvement becomes statistically possible. In this way, all manner of wondrous things are supposed to evolve bit by tiny bit.

However, I am seeing irreducible complexity all over the place these days. For example, your upper-jaw dentition must mesh pretty accurately with that of your lower jaw or you can't eat. Thus, the process of evolutionary foreshortening of the muzzle of the great apes to the flat human face could never have happened, assuming that a single mutation affects only the upper or lower jaw. But it did. (Let us gloss over the fact that that is an assumption, because the contrary seems to require non-local rules in development.)

Furthermore, how can any instinctive signaling system evolve one mutation at a time? At a minimum, you always need both the transmitter adaptation and the receiver adaptation, not to mention further mutations to connect the receiver circuit to something useful. The evolution of altruism presents a similar problem. The lonely first altruist in the population is always at a disadvantage in competition with the more selfish non-mutants unless it also has a signaling system that lets it recognize fellow altruists (initially, close relatives) and a further mutation that places the altruistic behavior under the control of the receiver part of this system. Thus, altruists would only be altruistic to their own kind, the requirement for altruism to be selected in the presence of selfishness. Finally, the various parts of this system must be indissolubly linked in a way that the non-altruists cannot fake.

My solution is to label the crossing-over events that occur during meiosis as "tetra-mutations." In crossing over, two homologous chromosomes pair up along their length and swap a long segment of DNA, a process requiring four double chain breaks and their corresponding repairs. Because of the presence of single-nucleotide polymorphisms, the homologous chromosomes are not exactly the same, so that each of the upstream sides of the four chain breaks ends up in a subtly different genetic environment. If the break point falls between a cis-acting regulatory element and the corresponding structural gene, for instance, the former may now control the expression of a slightly different protein. Thus, there could be as many as four distinct functional consequences of one crossing-over event. Why not call that a tetra-mutation?

In this way, a concerted change affecting four distinct sites becomes possible. The two ends of the recombinant segment can in principle be functionally unrelated initially. They become related if both are affected by the same tetra-mutation and the entire change increases fitness and is thus selected.

A single tetra-mutation could in principle produce viable altruism at one stroke because of the number of simultaneous changes involved. 

The probability of a combination of simultaneous local changes being beneficial to the organism is much smaller on mathematical grounds than is the probability of a given single-nucleotide change being beneficial. However, these unfavorable statistics are at least partly offset by the existence of a dedicated system for producing tetra-mutations in large numbers, namely meiosis, part of the process of maturation of egg cells and sperm cells.

In the big picture, tetra-mutations provide a way for a species to discontinuously jump into new niches as they open up, possibly explaining how a capacity for this kind of mutation could spread and become characteristic of surviving species over time. This idea also provides a ready explanation for the lack of transitional forms in the fossil record.

5-30-2018: Here is the search description again, in case you missed it or could not see all of it: Sexual reproduction may allow the evolution of irreducible complexity by increasing the intrinsic complexity of the basic building block of change, the mutation.

6-12-2018: Upon further reflection, it seems that the tetramutation construct described above lacks validity because during gamete maturation it falls apart into two bi-mutations, both of which cannot contribute to the same zygote. The bi-mutation is stable, however, because of the intervening translocated DNA segment. It is harder to see how a complex adaptation like altruism could evolve out of nothing but mono-mutations and bi-mutations, but that does not mean the theory put forward in this post is necessarily wrong. One must not argue from lack of imagination. It is an interesting question, actually, what is the minimum set of all mutation types necessary to account for all known adaptations.

8-27-2019: In my ignorance, I have undersold the bi-mutation idea. A very far-reaching change to the genetic information can occur during crossing-over that is not at all subtle and is termed unequal crossing-over. This form of the process arises because of inaccuracies, sometimes major, in the initial alignment of the homologous chromosomes prior to crossing-over. When the process is finished, one chromosome has been shortened and the other has been lengthened, with gene duplication. This is the major source of gene duplication, which, in turn, is a major source of junk DNA, the part that is classified as broken genes. Two questions come to mind. The first is, are anatomical features such as jaw length and axon targets somehow controlled by variations in gene dose? The second, which is a tangent, is, are broken genes really broken or just temporarily switched off by genetic drift at some mutational hot spot in the recognition site of some transcription factor? The analogy here is to a generator in a power plant that has been placed in stand-down mode because of a temporary decrease in the demand for electrical power.

#34. Emotions [evolutionary psychology, genetics, neuroscience]

EP    NE    GE

Red, theory; black, fact.

12-17-2017: In previous posts, I theorized that humans, along with all other sexually-reproducing species, have a long-range guidance system that I called proxy natural selection, or preferably, post-zygotic gamete selection (PGS), that is basically a fast form of evolution in which individual cells, the gametes, are the units of selection, not individuals. Selection is conjectured to happen post-zygotically (i.e., sometime after the beginning of development, or even in adulthood) but is retroactive to the egg and sperm that came together to create the individual. Each gamete is potentially unique because of the crossing-over genetic rearrangements that happen during its maturation. This theory explains the biological purpose of this further layer of uniqueness beyond that due to the sexual mixing of chromosomes, which would otherwise appear to be redundant.

Our emotions are conjectured to be programmed by species-replacement group selection and to serve as proxies for increases and decreases in the fitness of our entire species.

A further correlate of an emotion beyond the cognitive and autonomic-nervous-system components would be the neurohumoral component, expressed as chemical releasing and inhibiting factors that enter the general circulation via the portal vessels of the hypothalamus, blood vessels which are conventionally described as affecting only the anterior pituitary gland. These factors are theorized to reach the stem-like cells that mature into egg and sperm, where they set reversible epigenetic controls on the level of crossing-over that will occur during differentiation. Large amounts of crossing-over are viewed as retroactively penalizing the gametes leading to the individual by obfuscating or overwriting with noise specifically the genetic uniqueness of said original gametes. In contrast, low levels of further crossing-over reward the original gametes with high penetrance into the next generation. Here, I believe you have all the essential ingredients of classical natural selection, and all the potential, in a process that solves problems on an historical timescale.

Crossing-over happens only between homologous chromosomes, which are the paternal and maternal copies of the same chromosome. Human cells have 46 chromosomes because they have 23 pairs of homologous chromosomes. The homologous-chromosome-specificity of crossing-over suggests that the grand optimization problem that is human evolution has been broken down into 23 smaller sub-problems for the needs of the PGS process, each of which can be solved independently, without interactions with any of the other 22, and which involves a 23-fold reduction in the number of variables that must be simultaneously optimized. In computing, this problem-fragmentation strategy greatly increases the speed of optimization. I conjecture that it is one of the features that makes PGS faster than classical natural selection.

However, we now need 23 independent neurohumoral factors descending in the bloodstream from brain to testis or (fetal) ovary, each capable of setting the crossing-over propensity of one specific pair of homologous chromosomes. Each one will require its own specific receptor on the surface of the target oogonia or spermatogonia. Check this out in the literature, and you will already find a strange diversity of cell-surface receptors on the spermatogonia. (I haven't looked at oogonia yet.&&) I predict that the number of such receptors known to science will increase to at least 23. None of this is Lamarkism, because nervous-system control would be over the standard deviation of behavioral traits, not their averages.

1-09-2018: Naively, this theory also appears to require 23 second messengers to transfer the signals from cell surface to nucleus, which sounds excessive. Perhaps the second messengers form a combinatorial code, which would reduce the number required by humans to log2 (23) = 4.52, or 5 in round numbers. This is much better. Exactly five second-messenger systems are known, these being based on: cyclic AMP, inositol triphosphate, cyclic GMP, arachidonic acid, and small GTPases (e.g., ras). However, many mammalian species have many more than the 32 chromosome pairs needed to saturate a 5-bit address space.

1-10-2018: If we expand the above list of second messengers with the addition of the calcium/calmodulin complex, the address space expands to 64 pairs of homologous chromosomes, for a total ploidy of 128. This seems sufficient to accommodate all the mammals. Thus, a combinatorial second-messenger code representable as a five- or six-bit binary integer in most organisms would control the deposition of the epigenetic marks controlling crossing-over propensity.

If the above code works for transcription as well as epigenetic modification, then applying whatever stimuli it takes to produce a definite combinatorial second-messenger state inside the cell will activate one specific chromosome for transcription, so that the progeny of the affected cell will develop into whatever that chromosome specifies, be it an organ, a system, or something else. And there you may have the long-sought key to programming stem cells. You're welcome.

Each pair of homologous chromosomes may correspond to what in an earlier post was called a "PNS focus." The requirement that the evolution of each chromosome contribute independently to the total increase in fitness suggests that a chromosome specifies a system, like the nervous system or the digestive system. We seem to have only 11 systems, not 23, but more may be defined in the future.

A related concept is that a chromosome specifies an ancestral, generic cell type, like glial cells (4 subtypes known) or muscle cells (3 subtypes known). The great diversity of the neurons suggest that they must be reclassified into multiple basic types, perhaps along the lines suggested by the functional classification of the cranial nerves: general somatic, general visceral, and special somatic (i.e., specific senses).

1-09-2018: A third concept for function assignment to homologous pairs of chromosomes postulates a hypothetical maximally divided genome in which each cell type has its own chromosome pair, a state conjectured to seldom occur in nature. Co-evolution of clusters of cell types (e.g., neurons and glia; bone and cartilage) would create selection pressure for the underlying cell-type-specific chromosomes to become covalently linked into the larger chromosomes that we see in the actual karyotypes. Thus, each observed homologous pair would correspond to a few cell types that are currently co-evolving, which seems to return us to the system or organ concept. 

01-08-2019: The system specified by a chromosome may be called a cooperation system, and these may be organized in a hierarchy, following the general principles of spatial organization outlined in my post: "The Pictures in Your Head." Chromosomes activated earlier in development will specify system-like entities and those activated late in development will specify organ-like entities. Only the first-activated chromosome will apply to the entire organism.

Humans depend on complex social structures for their survival, and this comes out of our individual behavioral tendencies. Probably, most PGS adaptations to environmental fluctuations involve modifying these structures, which would come out of subtle modifications of individual behaviors. I think I am just repeating E.O. Wilson here. Our hard-wired species-fitness definitions would give rise to the primary emotions, perhaps in the hypothalamus or limbic system, by connecting specific stimuli to primary emotions in the manner of an if-then rule. 

Further out on the cortex, the specific stimuli being connected would get progressively more complex and learning-dependent, and progressively less concerned with the "what" of behavior (i.e., our species-specific taxes) and more with the "how" of behavior. In "how" mode, the complex stimuli become more like signposts to be consulted on a journey. PGS adaptations of our behavior would affect the hardwired aspects of this hypothetical transition zone. The primary emotions would then be like the highest hierarchical level of our motor program, or like the least-indented instructions of a conventional high-level computer program.

I conjecture that religion is important because it goes straight for this highest level. We all know that religion is kind of an emotional business, what with the organ music and the stained glass and all such as that, and this is why. I therefore conjecture that words spoken often from the pulpit, such as God, sin, forgiveness, devil, angel, soul, salvation, etc., all enclose a secret that writers such as Dawkins do not grasp: the emotions are the message. To illustrate this, let us attempt an emotional definition of the master symbol, "God."

God: feeling loved and secure to the point of invulnerability; feeling small in an agreeable way, as in the presence of mountains; feeling brotherly/sisterly towards one's fellow humans; blossoming in confidence into one's full potential; fearing nothing.

Perhaps that's enough to give the general idea. No doubt a whole dictionary could be compiled along these lines. When the priest strings these emotion-words together, he creates an experience for the congregation that could fairly be called a form letter from "God," assuming that the word "God" points to the PGS process itself. The job of the priest is to help the congregation relate on a deep level to the sacred texts and to see/feel how they apply to the challenges of the here and now.

7-05-2018: Another term for PGS would be "Yahwetion," from "Yahweh," the conventional modern spelling of the name of the god of ancient Israel, and the "tion" ending indicating a process, like evolution. This neologism advantageously steers people away from category errors like attempting to worship it, or appease it, or what have you.

The conventionally religious will complain that this would make prayer to God impossible, but not if prayer itself is re conceived as "auto socialization," following the educational theory of prayer. Then prayer becomes a fantasy conversation with anyone, living or dead, that you would like to have as a mentor, if it were possible.

#25. Proxy Natural Selection from the Inside [evolutionary psychology, genetics]

EP    GE    

Red, theory; black, fact.

My first post on proxy natural selection (PNS) left open some questions, such as what it should feel like, if anything, when one is fulfilling the species objective function and being deemed "proxy-fit" by one's own hypothalamus.

I conclude that it's just what you would think: you feel joy and/or serenity. Joy is one of Ekman's six basic universal human emotions, the others being fear, anger, disgust, sadness, and surprise. I think that emotions collectively are the operations of the highest-level human behavioral program. (That is, the program in its broadest outlines.) The unpleasant emotions force you to get off the couch until they are taken care of, and joy lets you get back on. Thus, the unpleasant four are the starting emotions, and joy is the stopping emotion. 

Surprise may be a meta-emotion that tells you that your threshold for experiencing one of the other emotions is too high, and immediately lowers it. I also think that each activation of an emotion tends to lower the threshold for activating it next time, which implies a positive feedback loop capable of changing the personality to suit suddenly changed circumstances, especially if the emotion eventually begins issuing with no trigger at all.

To relate this to the mechanism of PNS, the crossing-over events that went into making the sperm cell that made you would theoretically affect brain development more than anything else, specifically connecting some random stimulus to one of the unpleasant primary emotions. This creates your temperament, and thus your personality, which is the unique quality which you have to offer the world, and on which you are being tested by history. If the actions to which your own, special bete noir propel you are what the species objective function is looking for, you succeed, feel joy and serenity, and experience an altered methylation status of the DNA in your spermatogonia, if you are male, which (I conjecture) suppresses further crossing over in the manufacture of your own sperm, so that your personality type breeds true, which is what the population needs. 

PNS is quickie evolution to respond to challenges that come and go on less than a multi-thousand generation timescale, and I conjecture that it explains the complexities of sexual reproduction. You may object that trees, for example, have no behavior, much less personalities, and yet they have sexual reproduction. However, trees probably adapt quickly not by behavioral change, but by changes in their chemistry. The chemistry in question would be the synthesis of pesticidal mixtures located in the central vacuole of each plant cell. In terms of such mixtures, each tree should be slightly unique, an easily testable prediction.

Here is my own self-analysis in terms of PNS theory. My special emotional novelty that is potentially my gift to the world is a morbid fear of social rejection. This has motivated much more than the usual self-criticism of my own creative productions before they are communicated to others, for fear of rejection, leading to the kind of thing you are now reading. Social rejection/criticism hits me like a wall of flame that burns for days, or like some kind of rays coming out of the other person's head. The rejection that goes with the dating game has made it intolerable to me, leading to a lifelong celibacy that has freed all my resources for scientific pursuits. 

My father was a general in the Canadian Armed Forces, and was most unlike this, but my older brother takes after him somewhat. What happened to sour my father's life so radically before my birth in 1953, so that his recombinotype (coined word) no longer bred true? I conjecture that it was the failure of the defeat of Nazi Germany to produce a true, lasting peace, only ushering in the nuclear cold war with the USSR. With this, "God" was telling us: "Don't study war no more."

Each of the four unpleasant "starting" emotions may sub serve one of the four pillars of the species objective function already listed in The intermind: Engine of History?. Thus: sadness, altruism; disgust, genetic diversity (due to point mutations; what is motivated here is the screening of such novelties, screening always being the expensive part); fear, memetic diversity (or motivating prescreening of memetic novelties); anger, dispersal. Each of these emotions seems to have another use, in preserving the life of the individual, as opposed to the entire species. Thus: sadness, unfavorable energy balance; disgust, steering one away from concentrations of harmful bacteria; fear, avoidance of injury and death; anger, driving away competitors for food and mates. 

#23. Proxy Natural Selection: The God-shaped Gap at the Heart of Biology [genetics, evolution]

EV    GE    

Red, theory; black, fact.

2-06-2017

As promised, here is my detailed and hypothetical description of the entity responsible for compensating for the fact that our microbial, insect, and rodent competitors evolve much faster than we do because of their shorter generation times. In these pages, I have been variously calling this entity the intermind, the collective unconscious, the mover of the zeitgeist, and the real, investigable system that the word "God" points to. I here recant my former belief that epigenetic marks are likely to be the basis of an information storage system sufficient to support an independent evolution-like process. I will assume that the new system, "proxy natural selection" (PNS) is DNA-based.

11-20-2017

The acronym PNS is liable to be confused with "peripheral nervous system," so a better acronym would be "PGS," meaning "post-zygotic gamete selection."

2-06-2017

First, a refresher on how standard natural selection works. DNA undergoes point mutations (I will deal with the other main type of mutation later) that add diversity to the genome. The developmental process translates the various genotypes into a somewhat diverse set of phenotypes. Existential selection then ensues from the interaction of these phenotypes with the environment, made chronically stringent by population pressure. Differential reproduction of phenotypes then occurs, leading to changes in gene frequencies in the population gene pool. Such changes are the essence of evolution.

PNS assumes that the genome contains special if-then rules, perhaps implemented as cis-control-element/structural gene partnerships, that collectively simulate the presence of an objective function that dictates the desiderata of survival and replaces or stands in for existential selection. A given objective function is species-specific but has a generic resemblance across the species of a genus. The genus-averaged objective function evolves by species-replacement group selection, and can thus theoretically produce altruism between individuals. The if-then rules instruct the wiring of the hypothalamus during development, which thereby comes to dictate the organism's likes and dislikes in a way leading to species survival as well as (usually) individual survival. Routinely, however, some specific individuals end up sacrificed for the benefit of the species.

Here is how PNS may work. Crossing-over mutations during meiosis to produce sperm increase the diversity of the recombinotypes making up the sperm population. During subsequent fertilization and brain development, each recombinotype instructs a particular behavioral temperament, or idiosyncratotype. Temperament is assumed to be a set of if-then rules connecting certain experiences with the triggering of specific emotions. An emotion is a high-level, but in some ways stereotyped, motor command, the details of which are to be fleshed out during conscious planning before anything emerges as overt behavior. Each idiosyncratotype interacts with the environment and the result is proxy-evaluated by the hypothalamus to produce a proxy-fitness (p-fitness) measurement. The measurement is translated into blood-borne factors that travel from the brain to the gonads where they activate cell-surface receptors on the spermatogonia. Good p-fitness results in the recombination hot spots of the spermatogonia being stabilized, whereas poor p-fitness results in their further destabilization. 

Thus, good p-fitness leads to good penetrance of the paternal recombinotype into viable sperm, whereas poor p-fitness leads to poor penetrance, because of many further crossing-over events. Changes in hotspot activity could possibly be due to changes in cytosine methylation status. The result is within-lifetime changes in idiosyncratotype frequencies in the population, leading to changes in the gross behavior of the population in a way that favors species survival in the face of environmental fluctuations on an oligogenerational timescale. On such a timescale, neither standard natural selection nor synapse-based learning systems are serviceable.

2-07-2017

The female version of crossing over may set up a slow, random process of recombination that works in the background to gradually erase any improbable statistical distribution of recombinotypes that is not being actively maintained by PNS.

7-29-2017

Here is a better theory of female PNS. First, we need a definition. PNS focus: a function that is the target of most PNS. Thus, in trees, the PNS focus is bio elaboration of natural pesticides. In human males, the PNS focus is brain development and the broad outlines of emotional reactivity, and thus behavior. In human females, the PNS focus is the digestive process. The effectiveness of the latter could be evaluated while the female fetus is still in the womb, when the eggs are developing. The proxy fitness measure would be how well nourished the fetus is, which requires no sensory experience. This explains the developmental timing difference between oogenesis and spermatogenesis. Digestion would be fine tuned by the females for whatever types of food happen to be available in a given time and place.

8-18-2017

Experimental evidence for my proposed recombination mechanism of proxy natural selection has been available since 2011, as follows:

Stress-induced recombination and the mechanism of evolvability

by Weihao Zhong; Nicholas K. Priest

Behavioral Ecology and Sociobiology, 03/2011, Volume 65, Issue 3

permalink:

http://ncsu.summon.serialssolutions.com/#!/search?bookMark=ePnHCXMwfV1NS8QwEC2yBz9-gxL0JgTytUl7EUQU767nkDQJeCgu7uLv903SVlEQepx0pmky8yaTvJx3G-StuZsLiKLydSpLO8QEx8Ry3J3QgR9Nmx6t2tAivxGcaNhOFw9qZd-fdXcv9bQER26Kr0yMMsQJ6WK1mCHPZoBIbMp0QvbtMLH3wjKm9GfjtwbEen163D088_lSAT4i9js-xgi_DdSQBplcwQhXIQSggNjHVEpwUlIlK-uSyJI4JMRspZKKymyzTfqiu27vXVy3n__6wQO9GARIQVXsqyZEbt7TWDl-hNEj1wHg2A5EOiqbwBIM_b6xS_iVR7h2mxcNpTtPN7vf_NIcIq2HjEeotopifT_8L_XDwNsmtZR_V_2ECDxpxqOr6m9j_wpDiOrp_r6N82bqPhW0uWxt6i7PtYGRhgh9lP4C2uagLw

Abstract:

"The concept of evolvability is controversial. To some, it is simply a measure of the standing genetic variation in a population and can be captured by the narrow-sense heritability (h2). To others, evolvability refers to the capacity to generate heritable phenotypic variation. Many scientists, including Darwin, have argued that environmental variation can generate heritable phenotypic variation. However, their theories have been difficult to test.

 Recent theory on the evolution of sex and recombination provides a much simpler framework for evaluating evolvability. It shows that modifiers of recombination can increase in prevalence whenever low fitness individuals produce proportionately more recombinant offspring. Because recombination can generate heritable variation, stress-induced recombination might be a plausible mechanism of evolvability if populations exhibit a negative relationship between fitness and recombination. Here we use the fruit fly, Drosophila melanogaster, to test for this relationship.

We exposed females to mating stress, heat shock or cold shock and measured the temporary changes that occurred in reproductive output and the rate of chromosomal recombination. We found that each stress treatment increased the rate of recombination and that heat shock, but not mating stress or cold shock, generated a negative relationship between reproductive output and recombination rate. The negative relationship was absent in the low-stress controls, which suggests that fitness and recombination may only be associated under stressful conditions. Taken together, these findings suggest that stress-induced recombination might be a mechanism of evolvability."

However, my theory also has a macro aspect, namely that the definition of what constitutes "stress," in terms of neuron interconnections or chemical signaling pathways, itself  evolves, by species-replacement group selection. Support for that idea is the next thing I must search for in the literature. &&