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.Because collagen is so widespread in the body, the generaldegradation of this "extracellular matrix" is thought by many to be amajor impediment to efficient functioning of many organs, and amajor contributor to overall senescence.Any or all of the above cellular changes could contribute signifi-cantly to the overall senescence of the organism.The array of changesin an organism resulting from senescence the "aging phenotype" isenormous and complex; the changes for humans listed in Table 1.1 arejust the tip of the iceberg.At the cellular level, the total number ofchanges is more limited, and the same changes are observed in virtu-ally all eukaryotes as they senesce, whether the cells in question arereplicating or not.The challenge for the biogerontologist is not onlyto untangle the causes of organismal senescence from one another, butto try to understand how they relate to underlying causes of cellularsenescence.And at the cellular level, where senescence is still multi-faceted, the task will be to determine which causes of senescence aretruly primary, and to understand their genetic and molecular basis.Then, and only then, will we truly understand the aging process.Thisinvestigation is well under way, and what we have learned so far isdescribed in the remainder of this book.39 3The Evolution ofSenescence and DeathA great many discussions about the evolution of senescencebegin with the question of how senescence could have evolved in thefirst place.This question has long puzzled some of the best thinkers inevolutionary biology and genetics.Senescence as we understand it ineukaryotes does not exist, or at least has never been reliably detected,in prokaryotic organisms.It seems to have evolved very early ineukaryotic history, close in time to their emergence from the prokary-otes and to the beginning of the use of sex in reproduction.From our understanding of the principles of evolution and naturalselection, it is easy to imagine how traits like increased physical vigor,better eyesight, or brighter plumage for attracting mates traits thatwould increase reproductive fitness or prolong the reproductive life-span of an individual organism could arise within, and eventuallycome to dominate, a breeding population.It is less obvious how some-thing like senescence which severely impairs an organism's abilityto function in its natural environment could have been positively A MEANS TO AN ENDselected under these same rules.As individuals get older, their abilityto find mates, reproduce, and, where necessary, care for offspring areall seriously impaired by aging.So how could genetic variants pro-moting aging ever have been selected in evolution?This mystery is compounded by the fact that, in the wild, most ani-mals do not live long enough to experience serious aging.They diefrom disease or predation long before they become noticeably old; formost species, elderly individuals can be found only in zoos or labora-tories.That means that the very thing natural selection is supposed toact upon rarely ever shows up in nature.Yet, if kept in zoos or labs, ani-mals definitely do age.But where did the genes responsible for agingcome from?To get around these problems, some of the early evolutionary the-orists proposed that certain traits may be selected for in evolution thatare contrary to the interests of the individual, as long as they benefitthe species to which the individual belongs.It was proposed that aslong as such traits ultimately enhanced the ability of members of thespecies to pass on their genes, the interests of the individual would beserved (albeit as part of a larger group), and thus such a mechanismwould be consistent with evolution via natural selection.The problem with such "group selectionist" theories is that there issimply no known mechanism whereby they could actually work.As wewill discuss in more detail in a moment, variants of existing genes arisewithin an individual organism.They either allow that individual tobreed more effectively, or they don't.If they do, the new variants can,as a result of enhanced breeding efficiency of the "founding" individ-ual and its offspring, over many generations come to be carried by asignificant number of other individuals in the species.If the new geneconfers no particular reproductive advantage, it may linger for awhile,but will be unlikely to spread very far into the rest of the species.If thenew gene decreases reproductive efficiency, it will quickly disappear.This is the only basis on which natural selection can operate.There issimply no way to imagine how a gene arising in an individual could beacted on by natural selection on behalf of a species as a whole.There is noway for nature to anticipate, at the point in time when a new geneticvariant arises, possible future advantages a gene might have for theentire species.Yet a decision about the value of the new variant mustbe made at the time that it arises.And this decision can be made only42 THE EVOLUTION OF SENESCENCE AND DEATHin terms of the individual in which it arises, or that individual's imme-diate offspring.Thus, while there exist several examples of genes thatwould seem to confer benefits to the species rather than the individ-ual, group selection as an explanation of their existence has been aban-doned by all serious evolutionists for lack of a reasonable mechanismto explain it.Genes, Mutations, and EvolutionBefore launching into a discussion of the evolution of senes-cence, let's take a brief moment to discuss the nature of genes, geneticmutations, and natural selection, which are the working componentsof evolution.We will discuss these topics here only in the broadest out-lines; more detailed explanations will be provided in connection withspecific examples as they arise.Genes are stretches of DNA that directthe production of proteins in a cell.Humans have approximately100,000 genes distributed over twenty-three pairs of chromosomesstored in the nucleus of each cell in the body.This collection of genesin its entirety is referred to as the genome.Every aspect of a cell's lifehistory is directed by proteins synthesized according to the instructionscontained in genes.A set of genes sufficient to provide all the proteinsneeded for the construction and operation of a complete organism iscontained in the genome copies stored in each cell.When an organ-ism reproduces, it transmits a copy of its genome to its offspringthrough the special subset of cells known as germ cells (sperm and ovain humans).The remaining cells of the body the somatic cells arenot involved directly in reproduction, but rather serve to support theability of the germ cells to transmit genes to the next generation.Mutations are alterations in DNA that change the nature of genesand thus of the proteins produced [ Pobierz całość w formacie PDF ]
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.Because collagen is so widespread in the body, the generaldegradation of this "extracellular matrix" is thought by many to be amajor impediment to efficient functioning of many organs, and amajor contributor to overall senescence.Any or all of the above cellular changes could contribute signifi-cantly to the overall senescence of the organism.The array of changesin an organism resulting from senescence the "aging phenotype" isenormous and complex; the changes for humans listed in Table 1.1 arejust the tip of the iceberg.At the cellular level, the total number ofchanges is more limited, and the same changes are observed in virtu-ally all eukaryotes as they senesce, whether the cells in question arereplicating or not.The challenge for the biogerontologist is not onlyto untangle the causes of organismal senescence from one another, butto try to understand how they relate to underlying causes of cellularsenescence.And at the cellular level, where senescence is still multi-faceted, the task will be to determine which causes of senescence aretruly primary, and to understand their genetic and molecular basis.Then, and only then, will we truly understand the aging process.Thisinvestigation is well under way, and what we have learned so far isdescribed in the remainder of this book.39 3The Evolution ofSenescence and DeathA great many discussions about the evolution of senescencebegin with the question of how senescence could have evolved in thefirst place.This question has long puzzled some of the best thinkers inevolutionary biology and genetics.Senescence as we understand it ineukaryotes does not exist, or at least has never been reliably detected,in prokaryotic organisms.It seems to have evolved very early ineukaryotic history, close in time to their emergence from the prokary-otes and to the beginning of the use of sex in reproduction.From our understanding of the principles of evolution and naturalselection, it is easy to imagine how traits like increased physical vigor,better eyesight, or brighter plumage for attracting mates traits thatwould increase reproductive fitness or prolong the reproductive life-span of an individual organism could arise within, and eventuallycome to dominate, a breeding population.It is less obvious how some-thing like senescence which severely impairs an organism's abilityto function in its natural environment could have been positively A MEANS TO AN ENDselected under these same rules.As individuals get older, their abilityto find mates, reproduce, and, where necessary, care for offspring areall seriously impaired by aging.So how could genetic variants pro-moting aging ever have been selected in evolution?This mystery is compounded by the fact that, in the wild, most ani-mals do not live long enough to experience serious aging.They diefrom disease or predation long before they become noticeably old; formost species, elderly individuals can be found only in zoos or labora-tories.That means that the very thing natural selection is supposed toact upon rarely ever shows up in nature.Yet, if kept in zoos or labs, ani-mals definitely do age.But where did the genes responsible for agingcome from?To get around these problems, some of the early evolutionary the-orists proposed that certain traits may be selected for in evolution thatare contrary to the interests of the individual, as long as they benefitthe species to which the individual belongs.It was proposed that aslong as such traits ultimately enhanced the ability of members of thespecies to pass on their genes, the interests of the individual would beserved (albeit as part of a larger group), and thus such a mechanismwould be consistent with evolution via natural selection.The problem with such "group selectionist" theories is that there issimply no known mechanism whereby they could actually work.As wewill discuss in more detail in a moment, variants of existing genes arisewithin an individual organism.They either allow that individual tobreed more effectively, or they don't.If they do, the new variants can,as a result of enhanced breeding efficiency of the "founding" individ-ual and its offspring, over many generations come to be carried by asignificant number of other individuals in the species.If the new geneconfers no particular reproductive advantage, it may linger for awhile,but will be unlikely to spread very far into the rest of the species.If thenew gene decreases reproductive efficiency, it will quickly disappear.This is the only basis on which natural selection can operate.There issimply no way to imagine how a gene arising in an individual could beacted on by natural selection on behalf of a species as a whole.There is noway for nature to anticipate, at the point in time when a new geneticvariant arises, possible future advantages a gene might have for theentire species.Yet a decision about the value of the new variant mustbe made at the time that it arises.And this decision can be made only42 THE EVOLUTION OF SENESCENCE AND DEATHin terms of the individual in which it arises, or that individual's imme-diate offspring.Thus, while there exist several examples of genes thatwould seem to confer benefits to the species rather than the individ-ual, group selection as an explanation of their existence has been aban-doned by all serious evolutionists for lack of a reasonable mechanismto explain it.Genes, Mutations, and EvolutionBefore launching into a discussion of the evolution of senes-cence, let's take a brief moment to discuss the nature of genes, geneticmutations, and natural selection, which are the working componentsof evolution.We will discuss these topics here only in the broadest out-lines; more detailed explanations will be provided in connection withspecific examples as they arise.Genes are stretches of DNA that directthe production of proteins in a cell.Humans have approximately100,000 genes distributed over twenty-three pairs of chromosomesstored in the nucleus of each cell in the body.This collection of genesin its entirety is referred to as the genome.Every aspect of a cell's lifehistory is directed by proteins synthesized according to the instructionscontained in genes.A set of genes sufficient to provide all the proteinsneeded for the construction and operation of a complete organism iscontained in the genome copies stored in each cell.When an organ-ism reproduces, it transmits a copy of its genome to its offspringthrough the special subset of cells known as germ cells (sperm and ovain humans).The remaining cells of the body the somatic cells arenot involved directly in reproduction, but rather serve to support theability of the germ cells to transmit genes to the next generation.Mutations are alterations in DNA that change the nature of genesand thus of the proteins produced [ Pobierz całość w formacie PDF ]