#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

#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.

#27. Why Organized Religion? Theory Two [evolutionary psychology]

EP

Red, theory; black, fact.

My last post about proxy natural selection (PNS) has directed me to emphasize emotion more in seeking explanations for human behavior. I now think of emotions as an "endophenotype," to use a term from functional magnetic resonance imaging, that provides a useful stepping stone from evolutionary arguments to explanations of our daily lives. I recently applied this insight to obtaining a second explanation of religion, alternative or parallel to the first one that I give in a previous post.

What is the mood or feel as you enter a place of worship and participate in the ceremonies conducted there? More than anything else, the mood is one of great reverence, as though one is in the presence of the world's most powerful king. Kings are supposed to "represent their race." However, I want to translate that statement into a sociobiological function assignment. My discussion "Proxy Natural Selection from the Inside" suggests a problem: if the emotional outlines of people's behavior is being partly randomized in each generation by recombination-type mutations, a consistent moral code seems impossible if we assume that morality comes mostly from peoples' inborn patterns of emotional reactivity, that is, the sum total of everyones' betes noir. The purpose of a king may be to find or at least coincide with societies' moral center of gravity, around which a formal, if temporary, moral code can be constructed. In a complex society, everyone must be "on the same page" for efficient interaction. 

The same problem no doubt recurs each time organisms come together to form a colony, or super-organism: the conflict between the need of a colony for coordination of colonists and the need of evolution for random variability. Such variability will inevitably affect the formulation and interpretation of the coordinating messages that the colonists exchange, like all their other inborn characteristics. 

Kingship comes the corrupting influence of personal power, leading to destructive, tyrannical governments. Replacing a real king with a pretend-king named "God" would seem to be the solution that accounts for organized religion, but then one loses all flexibility, the flexibility that goes with having a flesh-and-blood king who can change his predecessor's laws based on current popular sentiment.

However, human nature may well have a core-and-shell structure, with an "unchanging" core surrounded by a slowly changing shell. The former would be the species-specific objective function previously alluded to in post #16, and produced by species-replacement group selection within the genus, and the latter would be due to PNS, and would represent the stratagems hit upon by our ancestors to meet the demands of the objective function in our time and place. This shell part may account for cultural differences between countries. The core may be implemented in the hypothalamus of the brain, whereas the shell may be implemented in the limbic system. The core, being unchanging, could be taught by organized religion, whereas the shell could be codified by the more flexible institution of government. Though the core is unchanging overall, specific individuals will harbor variations in it due to point mutations (not part of PNS), necessitating the standardizing role of religion. Synaptic plasticity would then be used to cancel the point-mutational variation in the objective function.

This core  consists of four pillars, or themes: genetic diversity, memetic diversity, altruism, and dispersal. Our energetic investment in obtaining each item is to be optimized. To produce this, the church of my acquaintance is continually emphasizing, respectively, tolerance, creating beautiful things, charity, and justice. It's almost too neat, especially if we adopt the deeply cynical-sounding position that the demand for "justice" only polarizes groups to the point of schism and diaspora.

#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. &&

#7. What is Intelligence? Part I. DNA as Knowledge Base [genetics, engineering]

EN     GE     

Red: theory; black, fact.

I have concluded that the world contains three intelligences: the genetic, the synaptic, and the artificial. The first includes (See Deprecated, Part 10) genetic phenomena and is the scientifically-accessible reality behind the concept of God. The synaptic is the intelligence in your head, and seems to be the hardest to study and the one most in need of elucidation. The artificial is the computer, and because we built it ourselves, we presumably understand it. Thus, it can provide a wealth of insights into the nature of the other two intelligences and a vocabulary for discussing them.

Artificial intelligence systems are classically large knowledge bases (KBs), each animated by a relatively small, general-purpose program, the "inference engine." The knowledge bases are lists of if-then rules. The “if” keyword introduces a logical expression (the condition) that must be true to prevent control from immediately passing to the next rule, and the “then” keyword introduces a block of actions the computer is to take if the condition is true. Classical AI suffers from the problem that as the number of if-then rules increases, operation speed decreases dramatically due to an effect called the combinatorial explosion.

A genome can be compared to a KB in that it contains structural genes and cis-acting control elements.(CCEs). The CCEs trigger the transcription of the structural genes into messenger RNAs in response to environmental factors and these are then translated into proteins that have some effect on cell behavior. The analogy to a list of if-then rules is obvious. A CCE evaluates the “if” condition and the conditionally translated protein enables the “action” taken by the cell if the condition is true.

Note that the structural gene of one rule precedes the CCE of the next rule along the DNA strand. Surely, would this circumstance not also represent information? However, what could it be used for? It could be used to order the rules along the DNA strand in the same sequence as the temporal sequence in which the rules are normally applied, given the current state of the organism’s world. This seems to be a possible solution to the combinatorial explosion problem, leading to much shorter delays on average for the transcriptase complex to arrive where it is needed. I suspect that someday, it will be to this specific arrangement that the word “intelligence” will refer.

The process of putting the rules into such a sequence may involve trial-and-error, with transposon jumping providing the random variation on which selection operates. A variant on this process would involve stabilization by methylation of recombination sites that have recently produced successful results. These results would initially be encoded in the organism's emotions, as a proxy to reproductive success. In this form, the signal can be rapidly amplified by inter individual positive feedback effects. It would then be converted into DNA methylation signals in the germ line. (See my post on mental illness for possible mechanisms.) DNA methylation is known to be able to cool recombination hot spots.

A longer-timescale process involving meiotic crossing-over may create novel rules of conduct by breaking DNA between promoter and structural gene of the same rule, a process analogous to the random-move generation discussed in my post on dreaming. Presumably, the longest-timescale process would be creating individual promoters and structural genes with new capabilities of recognition and effects produced, respectively. This would happen by point mutation and classical selection.

How would the genetic intelligence handle conditional firing probabilities in the medium to low range? This could be done by cross linking nucleosomes via the histone side chains in such a way as to cluster the CCEs of likely-to-fire-next rules near the end of the relevant structural gene, by drawing together points on different loops of DNA. The analogy here would be to a science-fictional “wormhole” from one part of space to another via a higher-dimensional embedding space. In this case, “space” is the one-dimensional DNA sequence with distances measured in kilobases, and the higher-dimensional embedding space is the three-dimensional physical space of the cell nucleus.

The cross linking is presumably created and/or stabilized by the diverse epigenetic marks known to be deposited in chromatin. Most of these marks will certainly change the electric charge and/or the hydrophobicity of amino acid residues on the histone side chains. Charge and hydrophobicity are crucial factors in ionic bonding between proteins. The variety of such changes that are possible.

Mechanistically, there seems to be a great divide between the handling of high and of medium-to-low conditional probabilities. This may correspond with the usual block structure of algorithms, with transfer of control linear and sequential within a block, and by jump instruction between blocks.

Another way of accounting for the diversity of epigenetic marks, mostly due to the diversity of histone marks, is to suppose that they can be paired up into negative-positive, lock-key partnerships, each serving to stabilize by ionic bonding all the wormholes in a subset of the chromatin that deals with a particular function of life. The number of such pairs would equal the number of functions.

Their lock-key specificity would prevent wormholes, or jumps, from forming between different functions, which would cause chaos. If the eukaryotic cell is descended from a glob-like array of prokaryotes, with internal division of labor and specialization, then by one simple scheme, the specialist subtypes would be defined and organized by something like mathematical array indexes. For parsimony, assume that these array indexes are the different kinds of histone marks, and that they simultaneously are used to stabilize specialist-specific wormholes. A given lock-key pair would wormhole specifically across regions of the shared genome not needed by that particular specialist.

 A secondary function of the array indexes would be to implement wormholes that execute between-blocks jumps within the specialist's own program-like KB. With consolidation of most genetic material in a nucleus, the histone marks would serve only to produce these secondary kind of jumps while keeping functions separate and maintaining an informational link to the ancestral cytoplasmic compartment. The latter could be the basis of sorting processes within the modern eukaryotic cell.