<\/p>\n
With and Without Sex<\/b><\/p>\n
The rules of the evolutionary game are different in sexual and asexual communities, and consequences for the strategies by which the game is played are dramatic. \u00a0In a sexual community you can be pretty sure that if you succeed in mating and your offspring survive, then your genes have a future. \u00a0Some of them will continue on, and others will be out-competed, and some of them will succumb to genetic drift and disappear. \u00a0Successful individuals will pass a lot of their genes into the future, and unsuccessful individuals will leave only a few. \u00a0Conversely, looking back in time, you have two parents, four grandparents, eight great grandparents, etc. \u00a0By the time you get to 20 generations, that\u2019s a million people, and probably they\u2019re not all different. \u00a0(People marry their sixth and fifth and even fourth cousins all the time and never know it.)<\/p>\n
But in asexual communities (this may not be obvious) it\u2019s winner-takes-all. \u00a0If you have a stable colonty of a billion bacteria, the laws of population genetics (essentially just statistics) say that within 100 generations, descendents of all but one of that original population will have disappeared with no legacy. \u00a0Everyone alive 100 generations from now will have been descended from a single individual alive today. \u00a0Bacteria breed rapidly, and 100 generations of bacteria might be about two weeks.<\/p>\n
<\/p>\n
Aging in Bacteria<\/b><\/p>\n
Because of this winner-take-all competition, bacteria are using every trick in the book to get ahead, or even get a tiny edge. \u00a0For example, their genomes are far more compact and economical than yours and mine because the time it takes to copy the DNA can limit the speed of their reproduction. \u00a0One trick for getting ahead is asymmetric reproduction, and asymmetric reproduction was the first form of aging, the \u201cbirth of death\u201d if you will.<\/p>\n
Let\u2019s say you were one of these bacteria, trying to beat the billion-to-one odds and be the one and only great-grandfather of the future. \u00a0You want to split in two, and as quickly as possible. \u00a0The quicker you divide, the quicker your odds go from 1 in a billion to 2 in a billion. \u00a0You can do a little better yet if you divide asymmetrically, giving a little boost to one of your two progeny at the expense of the other. \u00a0If the lesser twin loses, it\u2019s no great loss–after all, losing is what you expected anyway. \u00a0But if the greater twin has a little extra juice, that could make all the difference. \u00a0This is especially true, since the better offspring of the better offspring is doubly endowed, and might have an advantage that grows from one generation to the next.<\/p>\n
Some rod-shaped bacteria actually perform this trick. \u00a0Each new half-rod has one end that used to be an end and one end that used to be a middle. \u00a0It retains a subtle memory of its history, and if it has recently come from an end, it is stronger than if it has recently come from a middle. \u00a0In this diagram, the generations of bacteria are arrayed as though they stayed close together, strung in a line. \u00a0This is just for illustration–in fact they are living and moving separately; but they retain a memory of where in the line they belong.<\/p>\n
<\/p>\n The bacteria whose virtual positions would have been on the ends are the strongest. \u00a0The ones in the middle become weaker and weaker, and eventually this lineage dies out. \u00a0This asymmetry in replication of bacteria is the oldest, most primitive form of senescence.<\/p>\n From here, it is a short step to an asymmetry that is more like parent and child. \u00a0The \u201cmother\u201d bacterium buds with a smaller version of herself, and again and again. \u00a0But the mother won\u2019t keep this up forever–if she is not first killed by something external, she will age–bacterial senescence<\/a>–and stop reproducing after awhile. \u00a0This is real, full-bore aging, in its earliest and most primitive instance.<\/p>\n <\/p>\n Aging in Protists<\/b><\/p>\n Protists<\/a> (or protoctists) are single-celled life but much larger and more complex than bacteria, the first eukaryotes<\/a>. \u00a0Aging and programmed death in protists is already highly-developed, multiformed, adaptive, and plastic in response to the environment–with all the ecological functions ascribed to aging in animals and plants. \u00a0I presume that aging was fully developed in this way long before there was multi-celled life. \u00a0There are two principal forms of programmed death in protists. \u00a0One is apoptosis<\/a>, and the other is cellular senescence<\/a> (telomere attrition).<\/p>\n <\/p>\n Apoptosis<\/b><\/p>\n Apoptosis, or cell suicide, was discovered in the 19th century, and for more than 100 years it was understood to be a multipurpose mode of eliminating cells in the body that are either diseased or merely unwanted. \u00a0Before a cell dies \u201cunwillingly\u201d of external causes (e.g., starvation), it goes to every extreme to keep itself alive. \u00a0All its protective machinery is engaged in high gear, and when it fails, it fails spectacularly. \u00a0The cell is in complete disarray. \u00a0Apoptosis is just the reverse. \u00a0When the cell receives a signal (either from the outside, or within) it begins an orderly process of closing down its operation, recycling its biochemical stores, and fading gentle into the that good night<\/a>. \u00a0The cell slices up its own DNA, digests its own proteins, and turns itself into useful pieces that other cells might ingest.<\/p>\n During development of the foetus in the womb, much of the body\u2019s shape is sculpted by subtraction (the way Michelangelo<\/a> did it). \u00a0For example, fingers on the hand take shape as cells in webs between the fingers eliminate themselves via apoptosis. \u00a0More surprisingly, the brain develops via a process of selection<\/a>. \u00a0Starting with a thousand times more neurons than it needs, they grow connections to one another, and those that remain poorly connected (almost all of them) die via apoptosis. \u00a0This process continues after birth, so that an adult has fewer brain cells than an infant. \u00a0It is unclear whether this should be regarded as an early form of aging or as part of ongoing brain development.<\/p>\n Later in life, cells that become cancerous detect that they are a danger to the body and fall on their swords, using apoptosis. \u00a0Cells that are infected with a virus similarly figure it out early and kill themselves to limit spread of the virus.<\/p>\n All this fits well with theory, and is easy to understand. \u00a0Somatic cells have no evolutionary future, no long-term interests of their own apart from the welfare of the body as a whole. \u00a0Since they share 100% of their genes with the germ line, they are happy to live and die as appropriate to the needs of the body.<\/p>\n But microbes are independent evolving units, and according to evolutionary theory they are locked in competition with one another. \u00a0A yeast cell would never voluntarily sacrifice its own chances for those of another yeast cell…or such was the thinking until 2004<\/a>.<\/p>\n Readers of this blog are familiar with Valter Longo<\/a> and his work on fasting and caloric restriction. \u00a0In the 1990s when Longo was a grad student at UCLA, he discovered that a starving colony of yeast cells adapts by pruning itself. \u00a095% of the cells die, not of starvation, but via apoptosis. \u00a0They digest themselves and turn themselves into food for the remaining 5%. \u00a0This was so surprising and counter to evolutionary theory, that early versions of his paper were dismissed and sent back to him with a patronizing message that there must be some error. \u00a0Time and again, he returned to the lab to measure all the different biophysical and biochemical signatures of apoptosis.<\/p>\n It was a great education for Longo, both in the biochemistry of apoptosis, and also in the politics of science. \u00a0By the time his paper was accepted for publication in the Journal of Cell Biology<\/a>, Longo was done with his PhD, done with his post-doc, and a young professor at University of Southern California. \u00a0And now, 11 more years out, there are many known examples<\/a> of apoptosis in protists, and the biology community acts as though \u201cwe always knew that.\u201d<\/p>\n <\/p>\n Cellular Senescense<\/b><\/p>\n Cellular senescence was discovered by Leonard Hayflick<\/a> in the early 1960s, and, like Longo, Hayflick had to overcome a great deal of skepticism and dogma to get his work accepted. \u00a0Before Hayflick, the flawed experiments of Alexis Carrel<\/a> had been accepted for half a century as proof that (even though bodies as a whole are subject to aging) cells could continue to propagate forever. \u00a0The mechanism behind the \u201cHayflick limit\u201d was discovered a few years by Carol Greider and Elizabeth Blackburn<\/a>. \u00a0Every time a cell divides, it loses a little DNA from the ends of its chromosomes, the telomeres<\/a>. \u00a0The telomere is made of repetitive DNA, and carries no information, so it can easily be replenished. \u00a0But, curiously, the enzyme that performs the replenishing (telomerase) is locked up epigenetically in most cells most of the time, and so the cells\u2019 telomeres are permitted to shrink until the chromosome becomes chemically unstable, and the cell dies.<\/p>\n The biology community discovered this phenomenon in multi-celled higher organisms, and had a ready explanation for cellular senescence. \u00a0Greider herself [1990<\/a>] supplied the rationale: \u00a0cells that divide too many times are probably dividing out of control. \u00a0They are cancerous, and cellular senescence is there to put a check on their rogue adventure. \u00a0This explanation is accepted overwhelmingly today, though there was never a shred of evidence for it<\/a>, and in fact cellular senescence in humans actually increases cancer risk<\/a>.<\/p>\n But long before there was cancer, before there were plants and animals, cellular senescence and the rationing of telomerase evolved in cilliates for quite another purpose. \u00a0Ciliates (e.g. paramecia) are some of the most \u201cadvanced\u201d protists. \u00a0Their cells are surrounded by tiny hair-like cila that they use like oars to propel themselves through the water, and do so in shockingly intelligent ways, pursuing food or fleeing from a predator or locating a mate<\/a>.<\/p>\n In most protist communities, sex is optional. \u00a0Reproduction is via meitosis, simple cell division. \u00a0Sex is an entirely separate function, accomplished via conjugation<\/a>, in which two cells of the same species sidle up to one another, merge their protoplasm, and then exchange DNA, with individual genes swapped between homologous chromosomes. \u00a0By the time that two individuals emerge from this process, they have lost their identities, so that each one is \u201chalf me and half you\u201d.<\/p>\n The key to understanding cell senescence is that, in ciliates, telomerase is kept under lock and key during the process of mitosis, so the telomeres are permitted to shorten in generation after generation of clones. \u00a0But during conjugation, telomerase is freely expressed, and telomeres are restored to their full length, ready for dozens or even hundreds of cell divisions.<\/p>\n What is the purpose of this form of aging? \u00a0There can be but one answer: \u00a0cell senescence evolved in ciliates in order to enforce the sharing of genes. \u00a0In an asexual community, competition is cutthroat, and the winner takes all. \u00a0In a sexual community, genes are combined and recombined, diversity reigns, and evolution can follow a far more creative path. \u00a0But what\u2019s to stop a particularly macho young stud from opting out of the sex game, reproducing fast and furious, regarding his co-conspirators only as competition and wiping them out? \u00a0All the diversity and potential of the community would be lost if this happens. \u00a0So cell senescence evolved to prevent rogue individuals from opting out of sexual sharing.<\/p>\n Aging in ciliates evolved for the purpose of promoting a diverse community and enhancing the evolutionary response in adapting to changing environments. \u00a0And in higher organisms, aging continues to function in these same ways.<\/p>\n <\/p>\n The Bottom Line<\/b><\/p>\n The present evolutionary theory of aging was formulated in the 1950s, before any of this was known. \u00a0It was designed to apply to higher animals that age gradually. \u00a0\u00a0Not even plants (which often don\u2019t age) were considered, let alone semelparity (instant death after reproduction) or any of the topics on this page–cellular senescence and apoptosis and asymmetric division in bacteria. \u00a0Hardly anyone ever notices that the standard theory assumes implicitly that aging evolved \u201clate\u201d (after the Cambrian explosion<\/a>) and for reasons that only apply to multi-celled.<\/p>\n Not only the function and mechanisms are the same, but many of the same genes that regulate aging in microbes also regulate aging in multi-celled animals and plants. \u00a0But if the currently-accepted theory of aging is correct, then\u00a0aging in one-celled life forms must be\u00a0completely unrelated to aging in higher organisms. \u00a0From our present vantage, this\u00a0seems absurd, but that\u2019s not the way it happened historically.<\/p>\n I believe that aging in one-celled and multi-celled life serves similar purposes to aging in microbes, and the purposes have to do with ecology. \u00a0One purpose is population regulation, to keep a population from outgrowing its food supply; the second is to promote diversity and evolutionary change, to keep the population adapting and innovating.<\/p>\n","protected":false},"excerpt":{"rendered":"![\"Rod-bacteria-multiply\"](\"https:\/\/scienceblog.com\/wp-content\/uploads\/sites\/2\/2015\/07\/Rod-bacteria-multiply.jpg\")
<\/a><\/p>\n![\"\"](\"http:\/\/www.microbiologybytes.com\/virology\/kalmakoff\/baculo\/pics\/Apoptosis.gif.pagespeed.ce.xjjHGwnrJy.gif\")
<\/p>\n![\"\"](\"https:\/\/upload.wikimedia.org\/wikipedia\/commons\/c\/cb\/Paramecium.jpg\")
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