Archive for the ‘Uncategorized’ Category
The Potential Role of Centrioles in Active or Passive Female Choice
In animals and some other groups in which centrioles are inherited through males, good centrioles may be what females/ova are commonly choosing for or being manipulated with sexually to provide offspring or the expectation of offspring with the ability to escape difficult conditions by dispersing in time, space and/or niche, hence yielding grand offspring. These are the 3M’s – maintenance, motility and mutability. Centrioles as cellular organelles provide maintenance (the aster which emerges from them nucleates the cytoskelton), hence the choice for more mature, healthier males. They provide motility (they form the base of flagella), hence the choice for songs, dances and nuptial flights. They also provide mutability (in the sense of differentiation in development because they determine the planes and directions of cell divisions affecting cytoplasmic heredity), hence the choice for complex, symmetrical ornaments – for example those peacocks’ tails. The dramatic colour patterns sometimes observed in complex, symmetrical ornaments may make the latter more likely to be noticed by females in active or passive choice. And since it may be unclear whether flagella actually contribute to motility at the organismic level, it may be that songs, dances and nuptial flights are simply another form of complex, symmetrical ornament, one in space and time outside the body instead of inside it.
Feminist Views on a Theory of Sexes, Sex and Sexual Selection
In an article in Biological Theory in 2019 on mating markets and in two posts here, one in September 2019 on the two-fold cost of sex and in May 2020 on mating markets, together I hope made clear that a single premise, if justified, could solve the three major evolutionary puzzles about sex. The premise is that in a dioecious population for example, i.e. one composed of males and females, the two are ecologically, i.e. naturally selected, to be somewhat different. That would solve:
a) the puzzle of what compensates for the two-fold cost of sex because of the advantages of specialization
b) the puzzle of why they engage in sex at all because such trade is a form of bet hedging which produces diversity reducing the risk of extinction, and
c) the puzzle of why they engage in sexual competition and selection and why it takes the form that it does because sexual competition and selection are conflict over the profits of the sexual trade and the form it takes depends on what the naturally-selected differences are.
However, there is one thing not discussed in any of the three (possible feminist views of such a theory) and one briefly discussed in the article (the potential role of centrioles) but not in the posts. The former is discussed here and the latter will be in a subsequent post.
As noted in the article and in the most recent post, if the naturally-selected sex allocation is with males/male gametes at high frequency but low quality, i.e. low per capita cost, and females/female gametes at low frequency but high quality, i.e. high per capita cost, then sexually males/male gametes would compete intrasexually for female mates/female gametes and females/female gametes would compete intersexually choosing high quality male mates/male gametes. Feminists might find both something to both dislike and to like about this explanation of “conventional” sex roles. On the one hand, one can imagine some people reacting, “I see, on this view the sexes are naturally different, well then that justifies etc.” On the other hand, in this scenario, females/female gametes choose not just as a side effect of high male/male gamete frequency, nor even necessarily because they invest more in each offspring, both of which theories are popular. They can choose because they are of higher quality, i.e. have more invested in them than do males/male gametes, and hence they can afford to choose. Of course, where the naturally-selected strategies are different – sex role reversed, or both sexes high quantity but low quality, or both high quality but low quantity, then sex roles would be different than the conventional ones. And as previously noted, if the naturally-selected population were for some reason completely out of sex allocation equilibrium, then sexual selection could restore it as, or perhaps even more easily than by Fisher’s principle.
Is the Chicken and Egg Problem Solvable?
Evolutionary biologists sometimes say that a chicken is just an egg’s way of making more eggs even though they in fact begin their story of “generation” with chickens making eggs rather than eggs making chickens! Developmental biologists on the other hand actually study how eggs make chickens. Meanwhile, a “chicken and egg problem” has become a synonym in popular usage for an unsolvable problem. So is the apocryphal chicken and egg problem solvable?
I don’t know whether it can or ever will be solved empirically. However, theoretically I think the key question is whether geological and physio-chemical processes originally created many small things or a few large ones. I think the former is far more likely. If so, then individual growth and development came first and demographic growth developed rather than demographic growth coming first and individual growth and development evolving. Eventually of course the circle was closed so that instead of individual growth and development being the end and demographic growth a means to that end, or demographic growth the end and individual growth and development a means to that end, both became ends and both a means to the other’s end.
Get Costs In!
A lesson can be drawn from Charnov who transformed Fisher’s sex ratio theory into sex allocation theory but unfortunately the lesson has generally not spread in evolutionary theory beyond that. The lesson is that costs as well as frequencies have to be included and every time one dives deeper, one finds both again. That is the case whether we are talking about evolutionary ecology (e.g. density-dependence), social evolution (e.g. sexual selection), the origin of life, the extended evolutionary synthesis or whatever. The same point can be put in a variety of ways – costs as well as frequencies, quality (qu) as well as quantity (qa), investing as well as spending, somatic as well as reproductive functions etc. need to be included.
Both are needed and every time we dig deeper we need both again:
e.g. density dependence traditionally is qa (r) vs qu (K) but then need qa & qu of both 1
e.g. sexual selection theories are qa or qu but need both for sexual and for natural selection 2
e.g. the ‘originals’ grew (qu) as well as coming to reproduce (qa) 3
e.g. development as well as evolution must become part of the modern evolutionary synthesis 4
1 Density-Dependent Selection Revisited: Mechanisms Linking Explanantia and Explananda. Biological Theory 11(2) 2016: 113-121.
2 Mating markets: A naturally selected sex allocation theory of sexual selection. Biological Theory 14(2) 2019: 103-111.
3 Origins and the Eco-Evo-Devo Problem. Biological Theory 1(2) 2006: 116-118.
4 Three Modes of Evolution by Natural Selection and Drift: A New Or an Extended Evolutionary Synthesis? Biological Theory 12(2) 2017: 67-71.
Florestan Fernandes at the University of Toronto
In the academic year 1969-70 as a new graduate student in Sociology at the University of Toronto I took a course in “Latin American Societies” taught by Prof. Florestan Fernandes. I had a strong interest in economic and social development in the “third world” as it was called it in those days. I had spent two years after my Bachelors degree in Psychology and English as a Canadian University Service Overseas volunteer (the Canadian version of the American Peace Corps) teaching in eastern Nigeria. I and other volunteers were horrified at the English curriculum in secondary schools and teacher training colleges. It was composed exclusively of English novels and poems. We took great pleasure in introducing the students to Nigerian novels and poetry such as Chinua Achebe’s novel Things Fall Apart and Wole Soyinka’s poetry which they very much enjoyed. (Soyinka later became the first African to win the Nobel Prize in Literature.) I had also travelled in South America in Ecuador, Peru, Bolivia, Paraguay and Brazil for some months. Another ex-volunteer who had been stationed there told me he thought that the people of the altiplano area there were the poorest in the world but I had told him I thought that those of the Sahelian area of Africa were so I decided to see for myself!
I had also been politically active in protesting the siege of Biafra and along with other ex-volunteers and others, in organizing a teach-in on “The Crisis in Development”. Rather than an afternoon or evening of lectures, we did the teach-in a different way. We organized four weeks of discussion groups in the community, churches, recreation centres and so on. Each of us led one group having produced four handbooks with readings and questions for discussion. A few of the readings were from works by Frantz Fanon and Ivan Illich.
I have fond memories of Prof. Fernandes and his lectures and was particularly impressed, not only by the content, but also by his academic rigour. He walked in each week and sat in a small circle with ten or so of us and read his lectures which he had previously written out in full. The lectures were eventually published in a book “The Latin American in Residence Lectures”, Toronto, University of Toronto, 1969-70 edited by Prof. Kurt Levy, a political science professor. I gather that I and another graduate student from the course assisted the editor with some comments. When Prof. Fernandes gave us pretty much free reign on topics for a paper for the course, I decide to follow up on my interest in Frantz Fanon and Ivan Illich on development and wrote arguing that there was a convergence of their views on autonomous development.
After another year, once my MA degree was completed, my interests took a somewhat different turn. I eventually wrote my PhD thesis on comparing theories of change in biology, psychology and the social sciences in the sociology department but with an interdisciplinary committee. Among other things I wrote a fairly widely cited article on “Sociocultural Evolution: An Untried Theory” on the idea that culture and social organization and not just genes “descend with modification”. For example, the languages within each of some two hundred language families have descended with modification from a common ancestral language. I taught at the University of Toronto, The University of Western Ontario (now Western University) and eventually returned to the University of Toronto as Associate Professor, then full Professor then Emeritus (retired) Professor even though I am still active. In 2010 I also published a book with Cambridge University Press, “Darwinian Sociocultural Evolution: Solutions to Dilemmas in Cultural and Social Theory”.
Looking back now on the paper I wrote for Prof. Fernandes’ course (which I actually managed to find a copy of when asked by Diogo Valença and which he had published translated into Portugese along with this note in Novos Olhares Socials – UFRB V 3(2) 2020) my most egocentric memory is that he tried to give me a grade of 100 to which the powers that be objected so I ended up with a grade of 90 which was fine with me! But reading through the paper now, I don’t think I would change the substance at all – autonomy in development is as important as ever. And today the pandemic problem (hopefully in the short run), and the climate crisis in the longer run, are the two most important problems facing us all. I have every confidence Prof. Fernandes would agree with that as well were he still with us.
More Transmissible Mutants of COVID-CoV-2 Likely to be Less Rather Than More Damaging
In a post here on May 3 and in a post on the on-line magazine TVOL here
(https://evolution-institute.org/gene-culture-and-potential-culture-gene-coevolution-the-future-of-covid-19/)
I suggested that the virus COVID-CoV-2 could well evolve to become more transmissible. Three broad classifications of mechanisms were mentioned – increases in maintenance, motility and mutability. This now seems to have occurred in London and south-east England although the mechanism remains unknown. This is not just an “I told you so” but also to add another prediction. Mutants of the virus that successfully spread are likely to cause the disease COVID-19 to become less rather than more damaging and fatal. This is because it is not in the virus’ interest to keep one down and unable to circulate let alone kill its victims along with itself.
What is the Objective of Life? Grand Offspring of Course.
An organism does not have a life cycle, it is a life cycle. What is its objective? Not simply a duplicate set of genes, that’s for sure. Consider a simple semelparous life cycle – i.e. one that grows and develops then produces offspring all at the end. When has that life cycle been repeated or reproduced? When some or all of the offspring have grown and developed then produced offspring of course – i.e. when grand offspring have been born.
The Use of Re in Forecasting COVID-19 is Misleading
John Simpson kindly drew my attention to the Oxford’s COVID-19 Evidence Service’s method of forecasting the epidemic using their basic reproductive number which in my view is misleading (see www.cebm.net/oxford-covid-19/) and search “when will it be over”).
Their widely cited R parameter is defined as the expected average number of individuals one individual will infect in a susceptible population. If the expected R, Re, is less than 1 they expect the infection to eventually die out; if it is greater than 1, they expect it will continue to spread exponentially in the absence of immunization.
This is somewhat misleading. Instead, the growth of a biological population such as the virus is commonly described with the density-dependent S-shaped logistic function:
which relates the rate of growth of a population such as the virus SARS-CoV-2 which causes the disease COVID-19 at time t (the tangent to the curve relating population size to time) to its existing population size Nt and two parameters – r, the intrinsic rate of increase, and K, the ceiling, i.e. the carrying capacity of the environment. Initially, logistic growth approximates exponential growth because the expression in square brackets approximates 1 and hence dNt/dt approximates rNt , the expression for exponential growth. The maximum growth rate (tangent to the curve) is at K/2 and the growth rate declines thereafter symmetrically with its previous increase until it reaches 0 at N = K where population size itself levels off. The reason is obvious. Once half of the carrying capacity of the environment i.e. the susceptible host population is reached, it becomes harder and harder for the virus to find additional hosts; infected individuals become less and less likely to encounter people to infect – sometimes referred to by epidemiologists as herd immunity.
It should be pointed out that Re would not be misleading if it was being assumed that frequent culture-gene coevolution was taking place as described here about five posts ago. If frequent, adaptive mutations were taking place among the viruses, selected for by our culturally spread methods to avoid it (social distancing, mask wearing etc.), then the viral population could potentially continue to grow exponentially even to the ceiling. That extreme at least is very unlikely. Genetic variants of the virus are known, but there is no knowledge that the ones identified have adaptive and certainly that much adaptive significance, as of yet anyway. In any case, they explicitly assume a homogeneous viral population
However, it should also be pointed out that none of this matters for now and for the near future at least. By the best evidence I have been able to find, no country is close to having half of their population infected except possibly farmed Mink in Denmark!
J. B. S. Hadane’s Biography
Lately I enjoyed reading Samanth Subramanian’s recently published biography of J. B. S. Haldane, A Dominant Character: The Radical Science and Restless Politics of J. B. S. Haldane published by W. W. Norton in 2020.
Haldane (1892-1964) is largely remembered today along with Ronald Fisher and Sewall Wright as forging the foundations of population genetics, commonly known as neo-Darwinism or “the modern synthesis” uniting Mendel’s theory of heredity with Darwin’s theory of evolution in the nineteen twenties and thirties. According to Subramanian, he got along well with both of them but they did not get along well with each other.
Haldane was obviously a memorable character. He grew up assisting his physiologist father and not uncommonly serving as a subject for his father’s research and continued that tradition in the first world war on the front with respect to the use of munitions and in the second world war experimenting on himself and others seeking solutions to a submarine disaster to the detriment of his health. His first marriage was something of a scandal as she was married with a son when they began their relationship; they were later divorced and he married a research assistant. He regretted never having children. He was always rebellious against authority whether at school, in the various academic institutions that employed him in Britain, and even in the first institute in India that he moved to at age 65 after the Suez crisis, eventually becoming an Indian citizen.
After the war, he was the most visible scientist of his time in Britain, always in demand as a popular writer, speaker and for guest appearances. His popular writings were usually on some scientific point while veering into politics. He was the recipient of many scientific honorary awards from the British, the French and the Americans. He opposed racism and at least coercive eugenics even though his forecast for the future included a lot of positive eugenics including eliminating congenital defects, choosing occupations one is genetically best suited for, in vitro fertilization, cloning and so on.
Haldane believed science, politics and ethics could not be disentangled. He was a member of the Communist Party of Great Britain and indeed was chair of the editorial board of the party’s paper, The Daily Worker when it was banned for a time. Lysenko and Stalin presented him with a dilemma – tension between his science and Lysenkoism. Although he quit the party in 1950, he never formally renounced Lysenko or Stalin. M15 assiduously followed him around and compiled a large file on him but there is no evidence that he was ever a Soviet spy. He even managed to stir up controversy after his death from cancer when John Maynard Smith, Haldane’s student and fellow communist for a time (Smith quit the party over Lysenko in 1948) reported that Haldane had anticipated Hamilton’s inclusive fitness principle by declaring that he would lay down his life for two siblings or four cousins.
Subramanian effectively admits that the terms “modern” and “synthesis” ring a little hollow these days in light of contemporary findings about epigenetic inheritance and the emphasis on ecology and development as well as heredity leading to calls for a “new” or an “extended” synthesis. Somehow I doubt that Haldane would have minded – he always welcomed unexpected findings.
A Debate Over Senescence
The debate over theories of senescence (commonly defined as a decrease in function with age) that has gone on in the pages of TREE (Trends in Ecology & Evolution) is interesting but I will not try to summarize all the arguments here, see [1-6]. The key issue dividing champions of Hamilton [1,4,6] versus those of Williams [2,3,5] seems to be whether extrinsic mortality must be condition-dependent to select for senescence [1,4,6] or whether it just has to be extrinsic period [2,3,5]. Many points could be made about either (and indeed about both) sides of this argument. It seems strange to see two of the great evolutionary biologists of their time pitted against each other by others, especially since according to the first side at least, Williams eventually agreed with Hamilton anyway. The debate seems to be all about time but what about space? If the discussion is all about extrinsic mortality, what about intrinsic mortality? Is there such a thing? There must be believed to be, otherwise why the need to distinguish some mortality as extrinsic? Intrinsic mortality sounds like senescence itself, but then it is supposed to be extrinsic mortality that selects for senescence so . . .? Density dependence is mentioned but the classic works that initiated modern discussions of it are not mentioned or cited [7,8]. It seems obvious to me that senescence is indeed density dependent [9,10].
Small organisms (which also tend to have short, fast life cycles and many small offspring), because of their disproportionate surface area (for a sphere = 4π r2), tend to consume (eat and excrete) more, depleting and degrading the external environment, and hence to suffer mortality from extrinsic causes (predation, parasites, accidents etc.) Large organisms (which also tend to have longer, slower life cycles and fewer, larger offspring capable of producing grand offspring), because of their disproportionate volume (for a sphere = 4/3π r3), tend to digest (break down and build up) more, depleting and degrading the internal environment, and hence to suffer mortality from intrinsic causes (developmental, physiological, behavioural etc.) i.e. senescence. The argument is that the former are adapted to low density (in per capita cost and/or frequency) relative to resources i.e. plentiful resources within a population, or among populations, growing ones with a history of catastrophes and hence consume/produce more. The latter are adapted to high density (in per capita cost and/or frequency) relative to resources i.e. scarce resources within a population, or among populations, declining ones with a history of bonanzas and hence digest/reproduce more – struggling morphologically, physiologically and behaviourally to build up mechanisms of escape in time, space and/or niche. Of course, further distinctions could be drawn. Somatic and reproductive and temporal and spatial properties of life cycles are not perfectly correlated. Density relative to antagonists matters too, low in that case being bad conditions and high good ones. It matters whether the consumption is by means of parasitism or predation and so on.
Evidence? Well, we have long known experimentally that caloric restriction among the small fast, forcing them to devote fewer resources to consumption and hence by implication more to digestion, increases lifespan. But don’t we also know that caloric expansion among the large slow, devoting more resources to consumption and hence by implication less to digestion, decreases lifespan (e.g. obesity among humans)? The slogan for such a density dependent theory of senescence might be mice get eaten while men get cancer!
Now of course this argument is about different life histories rather than about stages within life histories. But given that juveniles are obviously smaller and adults obviously larger, surely the analogous inference can be drawn from one to the other. Humans after all lavish food on their young even as they sometimes go without themselves. As adult humans we know that our young children get bug after bug (most of which they thankfully do not die of at least these days). But what do our parents die of? Number one is heart disease and number two is cancer. Thereafter there is in order a list of things [11] which similarly do not have obvious extrinsic causes.
References
1. Moorad, J. et. al. (2019) Evolutionary ecology of senescence and a reassessment of Williams’ “extrinsic mortality” hypothesis. Trends Ecol. Evol. 34, 519-530
2. Day, T. and Abrams, P.A. (2020) Density dependence, senescence and Williams’ hypothesis. Trends Ecol. Evol. 35, 300-302.
3. Kozlowski, J. et. al. (2020) Williams’ prediction will often be observed in nature. Trends Ecol. Evol. 35, 302-303.
4. Moorad J. et. al. (2020) George C. Williams’ problematic model of selection and senescence: time to move on. Trends Ecol. Evol. 35, 303-305.
5. da Silva, J. (2020) Williams’ intuition about extrinsic mortality was correct. Trends Ecol. Evol. 35, 378-379.
6. Moorad, J. et. al. (2020) Williams’ intuition about extrinsic mortality is irrelevant. Trends Ecol. Evol. 35, 379.
7. MacArthur R.H. (1962) Some generalized theorems of natural selection. Proc. Natl. Acad. Sci. 48, 1893-1897.
8. MacArthur, R.H. and Wilson, E.O. (1967) The Theory of Island Biogeography. Princeton University Press.
9. Blute, M. (2010) Darwinian Sociocultural Evolution: Solutions to Dilemmas in Cultural and Social Theory. Cambridge University Press.
10. Blute, M. (2016) Density-Dependent Selection Revisited: Mechanisms Linking Explanantia and Explananda. Biological Theory 11, 113-121.
11. National Vital Statistics Report. United States Life Tables (2019)
https://www.cdc.gov/nchs/data/nvsr/nvsr68/nvsr68_07-508.pdf
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