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

EV   GE

Red, theory; black, fact

2 x 2

The Key Insight

Sexual reproduction may allow the evolution of irreducible complexity by increasing the intrinsic complexity of the basic building block of change, the mutation.

Irreducible Complexity 

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. You have irreducible complexity if an advantageous evolutionary innovation requires two mutations,  but neither confers any advantage in isolation and so cannot be selected up to a sufficiently high frequency that the second mutation is likely to happen in the background of the first.

However, I am seeing irreducible complexity everywhere these days. 

Possible Cases of Irreducible Complexity

For example, your upper-jaw dentition must mesh 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. 

Furthermore, how can any biological 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.

A Solution   

Consider the crossing-over events that occur during meiosis as complex mutations: two changes to the genome from a single event, each corresponding to one end of the DNA segment that translocates. In crossing over, two homologous chromosomes pair up along their length and swap a long segment of DNA, a process requiring two double-chain breaks on each end, and their corresponding repairs. A very far-reaching change to the genetic information can occur during crossing-over that 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. 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.

A Mechanism for the Evolution of Complexity 

Anatomical features such as jaw length and axon targets may be controlled by variations in gene dose that originate in unequal crossing-over.

In this way, a concerted change affecting multiple 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 complex mutation and the entire change increases fitness and is thus selected.

A single complex mutation could in principle produce a communication channel at one stroke because of the number of simultaneous changes involved. 

Statistical Issues

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 unfavourable statistics are at least partly offset by the existence of a dedicated system for producing complex mutations in large numbers, namely meiosis, part of the process of maturation of egg and sperm cells.

The Big Picture 

Complex 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 another explanation for the lack of transitional forms in the fossil record.

#37. The Fallacy of Justice [evolutionary psychology]

EP

Red, theory; black, fact

The Biology of Badness

Evil and criminality may sub-serve either dispersal or preemptive population reduction, both valuable biological processes that tend to prolong the survival of species. 

The algorithms for achieving these ends would have been created over time by some form of evolution.

Evolution and the Role of Emotion

The genetically inherited parts of our behavior enter consciousness as emotions, and can therefore be easily identified. The main outlines of civilization are probably due to the inherited behavior component, and not to the reasoning, conscious mind, which is often just a detail-handler. How could civilization rest on a process that can't even remember what happened last weekend?

Thus, humans have a dual input to behavior, emotion and reason. The above arguments show that evil and criminality come from the emotional input. Yet the entire deterrence theory of justice assumes the opposite, by giving the person a logical choice: "You do this, we do that, and you won't like it. So you don't do this, right?"

However, I think that people commit crimes for emotional reasons. As usual, the criminal's reasoning faculties are just an after-the-decision detail handler. The direction that this detail handler then takes is fascinatingly monstrous, but this does not mean that crime begins in reason.

Conclusion: the deterrence theory of justice is based on a category error.

Past and Future Responses to Badness

Religion, with its emphasis on emotion, was all the formal "law enforcement system" anyone needed up until only about 200 years ago, at the industrial revolution. We may be able to go beyond where religion takes us by means of a disease model of criminality.

It does make some sense to lock criminals up, because with less freedom they cannot physically commit as many crimes. Many prisons become dungeons, however, because of the public's desire for revenge. However, all revenge-seeking belongs to the dispersal/depopulation dynamic and is thus part of the problem. A desire for revenge may follow a crime very predictably, but logically, it is a non-sequitur.

A more nuanced theory of crime prevention is possible, where logical and technological constraints on behavior complement efforts to reduce the motivation for committing crimes at the source: the individual's perception of the fairness of society, which will be due to a combination of objective realities and the filters through which they are viewed. However, I originally wrote as I did because I don't think that logical and technological constraints are the squeaky wheel at the moment.

#35. The Thought Process Through the Ages [evolutionary psychology]

EP

Red, theory; black, fact

In the beginning, there was theology. At some point, intellectual endeavor split into wrestling with reality questions vs. morality questions. Then people had to figure out when to go with your gut and when not to.

_________________

Thought sources	Inputs	Output insights
		Reality (What is)	Blend	Morality (Thus…)
PGSd+senses	Emotion	politicsc		religionc
	Blend	astrologyb ↕	← theologya →	Jewish lawb ↕
Education+senses	Reason	sciencec		lawc

a. primordial condition

b. output distinction added

c. input distinction added

d. evolution; see post 22

If politics and science seem like strange bedfellows, consider that ancient rulers used to consult astrologers before making major decisions.

Just as emotion must not be allowed to contaminate scientific thought, is it equally true that reason must not be allowed to contaminate religious thought? Is failure to observe this restriction the cause of religious schisms?

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

EP   NE   GE

Red, theory; black, fact

A Genetics Theory 

All sexually reproducing species may have a long-range guidance system that that could be called proxy natural selection, or preferably, post-zygotic gamete selection (PGS). This is basically a fast form of evolution in which particular body 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.

Emotions Represent Fitness 

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.

The Corresponding Mechanistic Theory 

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 may 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 we have all the essential ingredients of classical natural selection, and all the potential, in a process that solves problems on an historical timescale.

The Limited Scope of Crossing-over

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.

Do Chromosome-specific Signaling Pathways Exist?

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. In the literature, I already find a strange diversity of cell-surface receptors on the spermatogonia. 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 traits, not their averages.

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. Five second-messenger systems are known, these being based on: cyclic AMP, inositol triphosphate, cyclic GMP, arachidonic acid, and small GTPases (e.g., ras). The AND-element that would be required for decoding could be implemented straightforwardly as a linear sequence of transcription-factor binding sites along the DNA strand. However, many mammalian species have many more than the 32 chromosome pairs needed to saturate a 5-bit address space. 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.

It Gets Bigger

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.

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.

Illustration credit: By Edmund Beecher Wilson - Figure 2 of: Wilson, Edmund B. (1900) The cell in Development and Inheritance (2nd ed.), Category:New York: The Macmillan Company, Public Domain, https://commons.wikimedia.org/w/index.php?curid=3155599

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

EV   GE

Red, theory; black, fact

The Problem and My Solution 

Some entity must be 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, "post-zygotic gamete selection" (PGS) is DNA-based.

Background 

First, a refresher on how standard natural selection works. DNA undergoes various mutations 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.

My Solution, Big Picture 

PGS 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.

The PGS Mechanism 

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 oligo-generational timescale. On such a timescale, neither standard natural selection nor synapse-based learning systems are serviceable.

Female PGS Is Different 

However, egg cells mature in utero and therefore face a selection disconnect or delay. 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 PGS.

A Better Theory of Female PGS 

First, a definition. PGS focus: a function that is the target of most PGS. Thus, in trees, the PGS focus might be bio-elaboration of natural pesticides. In human males, the PGS focus might be brain development and the broad outlines of emotional reactivity, and thus behaviour. In human females, the PGS focus might be 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.

Experimental evidence for the proposed recombination mechanism of PGS 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

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 signalling pathways, itself  evolves, by species-replacement group selection.