banner



Home  ›  Advantages And Disadvantages Of Mutation

Advantages And Disadvantages Of Mutation

Written By Tuesday, October 18, 2022 Add Comment Edit

How sexually reproducing multicellular organisms could accept evolved from a common ancestor species

Sexual reproduction is an adaptive feature which is common to almost all multicellular organisms and diverse unicellular organisms, with some organisms being incapable of asexual reproduction. Prior to the advent of sexual reproduction, the adaptation process whereby genes would change from 1 generation to the next (genetic mutation) happened very slowly and randomly. Sex evolved every bit an extremely efficient mechanism for producing variation, and this had the major advantage of enabling organisms to accommodate to changing environments. Sex did, nonetheless, come with a cost. In reproducing asexually, no fourth dimension nor energy needs to be expended in choosing a mate. And if the surroundings has non changed, then there may exist little reason for variation, equally the organism may already be well adapted. Sex also halves the corporeality of offspring a given population is able to produce. Sex, however, has evolved equally the nigh prolific means of species branching into the tree of life. Diversification into the phylogenetic tree happens much more apace via sexual reproduction than information technology does by manner of asexual reproduction.

Evolution of sexual reproduction describes how sexually reproducing animals, plants, fungi and protists could have evolved from a mutual ancestor that was a single-celled eukaryotic species.[1] [ii] [3] Sexual reproduction is widespread in the Eukarya, though a few eukaryotic species take secondarily lost the ability to reproduce sexually, such as Bdelloidea, and some plants and animals routinely reproduce asexually (past apomixis and parthenogenesis) without entirely having lost sex. The evolution of sexual activity contains 2 related yet distinct themes: its origin and its maintenance.

The origin of sexual reproduction can exist traced to early prokaryotes, around two billion years ago (Gya), when bacteria began exchanging genes via conjugation, transformation, and transduction.[4] Though these processes are distinct from truthful sexual reproduction, they share some bones similarities. In eukaryotes, true sex is thought to have arisen in the final eukaryotic common ancestor, possibly via several processes of varying success, so to have persisted (compare to "LUCA").[5]

Since hypotheses for the origin of sexual activity are difficult to verify experimentally (outside of evolutionary ciphering), most electric current piece of work has focused on the persistence of sexual reproduction over evolutionary time. The maintenance of sexual reproduction (specifically, of its dioecious form) by natural pick in a highly competitive world has long been one of the major mysteries of biology, since both other known mechanisms of reproduction – asexual reproduction and hermaphroditism – possess apparent advantages over it. Asexual reproduction can go along past budding, fission, or spore formation and does not involve the spousal relationship of gametes, which appropriately results in a much faster rate of reproduction compared to sexual reproduction, where l% of offspring are males and unable to produce offspring themselves. In hermaphroditic reproduction, each of the two parent organisms required for the formation of a zygote tin provide either the male or the female gamete, which leads to advantages in both size and genetic variance of a population.

Sexual reproduction therefore must offering meaning fitness advantages because, despite the two-fold cost of sex (come across below), it dominates among multicellular forms of life, implying that the fitness of offspring produced by sexual processes outweighs the costs. Sexual reproduction derives from recombination, where parent genotypes are reorganized and shared with the offspring. This stands in contrast to single-parent asexual replication, where the offspring is ever identical to the parents (barring mutation). Recombination supplies 2 fault-tolerance mechanisms at the molecular level: recombinational DNA repair (promoted during meiosis because homologous chromosomes pair at that time) and complementation (as well known equally heterosis, hybrid vigor or masking of mutations).

Historical perspective [edit]

Reproduction, including modes of sexual reproduction, features in the writings of Aristotle; modern philosophical-scientific thinking on the problem dates from at least Erasmus Darwin (1731–1802) in the 18th century.[six] August Weismann picked up the thread in 1885, arguing that sex serves to generate genetic variation, as detailed in the majority of the explanations below.[7] On the other hand, Charles Darwin (1809–1882) ended that the event of hybrid vigor (complementation) "is amply sufficient to account for the … genesis of the two sexes".[eight] This is consistent with the repair and complementation hypothesis, described below. Since the emergence of the modern evolutionary synthesis in the 20th century, numerous biologists including Westward. D. Hamilton, Alexey Kondrashov, George C. Williams, Harris Bernstein, Carol Bernstein, Michael Grand. Cox, Frederic A. Hopf and Richard E. Michod – take suggested competing explanations for how a vast array of different living species maintain sexual reproduction.

Advantages of sexual practice and sexual reproduction [edit]

The concept of sexual activity includes 2 fundamental phenomena: the sexual process (fusion of genetic information of two individuals) and sexual differentiation (separation of this data into two parts). Depending on the presence or absence of these phenomena, all of the existing forms of reproduction can exist classified as asexual, hermaphrodite or dioecious. The sexual process and sexual differentiation are unlike phenomena, and, in essence, are diametrically opposed. The get-go creates (increases) diversity of genotypes, and the second decreases information technology by half.

Reproductive advantages of the asexual forms are in quantity of the progeny, and the advantages of the hermaphrodite forms are in maximal diversity. Transition from the hermaphrodite to dioecious state leads to a loss of at to the lowest degree half of the diversity. So, the principal claiming is to explain the advantages given by sexual differentiation, i.eastward. the benefits of two separate sexes compared to hermaphrodites rather than to explain benefits of sexual forms (hermaphrodite + dioecious) over asexual ones. It has already been understood that since sexual reproduction is not associated with any articulate reproductive advantages, as compared with asexual, there should exist some important advantages in development.[nine] [ better source needed ]

Advantages due to genetic variation [edit]

For the reward due to genetic variation, there are three possible reasons this might happen. First, sexual reproduction can combine the effects of two beneficial mutations in the same individual (i.e. sexual practice aids in the spread of advantageous traits). Besides, the necessary mutations do not have to take occurred one after another in a single line of descendants.[ten] [ unreliable source? ] 2d, sex acts to join currently deleterious mutations to create severely unfit individuals that are then eliminated from the population (i.due east. sex aids in the removal of deleterious genes). Even so, in organisms containing only i set of chromosomes, deleterious mutations would be eliminated immediately, and therefore removal of harmful mutations is an unlikely benefit for sexual reproduction. Lastly, sex activity creates new gene combinations that may be more fit than previously existing ones, or may simply pb to reduced competition amid relatives.

For the reward due to DNA repair, there is an immediate big benefit of removing DNA damage by recombinational DNA repair during meiosis, since this removal allows greater survival of progeny with undamaged DNA. The advantage of complementation to each sexual partner is avoidance of the bad effects of their deleterious recessive genes in progeny by the masking outcome of normal dominant genes contributed past the other partner.[ citation needed ]

The classes of hypotheses based on the creation of variation are further broken downwards below. Any number of these hypotheses may exist truthful in any given species (they are non mutually exclusive), and unlike hypotheses may utilise in different species. However, a enquiry framework based on creation of variation has nonetheless to be institute that allows one to determine whether the reason for sexual activity is universal for all sexual species, and, if not, which mechanisms are interim in each species.

On the other manus, the maintenance of sex activity based on Deoxyribonucleic acid repair and complementation applies widely to all sexual species.

Protection from major genetic mutation [edit]

In contrast to the view that sex promotes genetic variation, Heng,[xi] and Gorelick and Heng[12] reviewed evidence that sex really acts as a constraint on genetic variation. They consider that sex activity acts as a coarse filter, weeding out major genetic changes, such every bit chromosomal rearrangements, but permitting small-scale variation, such as changes at the nucleotide or gene level (that are often neutral) to pass through the sexual sieve.

Novel genotypes [edit]

This diagram illustrates how sex might create novel genotypes more speedily. Two advantageous alleles A and B occur at random. The two alleles are recombined rapidly in a sexual population (meridian), only in an asexual population (bottom) the ii alleles must independently arise because of clonal interference.

Sexual activity could be a method by which novel genotypes are created. Because sex combines genes from two individuals, sexually reproducing populations can more easily combine advantageous genes than can asexual populations. If, in a sexual population, 2 different advantageous alleles arise at different loci on a chromosome in unlike members of the population, a chromosome containing the two advantageous alleles can exist produced within a few generations past recombination. Withal, should the same two alleles arise in different members of an asexual population, the simply way that one chromosome can develop the other allele is to independently gain the same mutation, which would take much longer. Several studies take addressed counterarguments, and the question of whether this model is sufficiently robust to explain the predominance of sexual versus asexual reproduction remains.[13] : 73–86

Ronald Fisher also suggested that sex might facilitate the spread of advantageous genes by allowing them to improve escape their genetic surroundings, if they should arise on a chromosome with deleterious genes.

Supporters of these theories answer to the balance argument that the individuals produced past sexual and asexual reproduction may differ in other respects too – which may influence the persistence of sexuality. For instance, in the heterogamous water fleas of the genus Cladocera, sexual offspring form eggs which are better able to survive the winter versus those the fleas produce asexually.

Increased resistance to parasites [edit]

One of the most widely discussed theories to explain the persistence of sex is that it is maintained to assist sexual individuals in resisting parasites, too known as the Blood-red Queen Hypothesis.[fourteen] [13] : 113–117 [15] [xvi] [17]

When an environs changes, previously neutral or deleterious alleles can become favourable. If the environment changed sufficiently rapidly (i.due east. between generations), these changes in the surround can make sex advantageous for the individual. Such rapid changes in surround are caused by the co-development betwixt hosts and parasites.

Imagine, for example that there is one factor in parasites with two alleles p and P conferring 2 types of parasitic ability, and 1 gene in hosts with 2 alleles h and H, conferring two types of parasite resistance, such that parasites with allele p can attach themselves to hosts with the allele h, and P to H. Such a situation volition lead to cyclic changes in allele frequency – as p increases in frequency, h volition be disfavoured.

In reality, there volition be several genes involved in the relationship betwixt hosts and parasites. In an asexual population of hosts, offspring will only have the different parasitic resistance if a mutation arises. In a sexual population of hosts, withal, offspring volition have a new combination of parasitic resistance alleles.

In other words, like Lewis Carroll's Ruby-red Queen, sexual hosts are continually "running" (adapting) to "stay in one place" (resist parasites).

Prove for this explanation for the development of sex is provided by comparison of the rate of molecular evolution of genes for kinases and immunoglobulins in the immune arrangement with genes coding other proteins. The genes coding for immune system proteins evolve considerably faster.[18] [19]

Farther evidence for the Ruddy Queen hypothesis was provided by observing long-term dynamics and parasite coevolution in a "mixed" (sexual and asexual) population of snails (Potamopyrgus antipodarum). The number of sexuals, the number asexuals, and the rates of parasite infection for both were monitored. It was found that clones that were plentiful at the beginning of the study became more susceptible to parasites over fourth dimension. Equally parasite infections increased, the once plentiful clones dwindled dramatically in number. Some clonal types disappeared entirely. Meanwhile, sexual snail populations remained much more stable over time.[20] [21]

Nonetheless, Hanley et al.[22] studied mite infestations of a parthenogenetic gecko species and its ii related sexual ancestral species. Contrary to expectation based on the Red Queen hypothesis, they found that the prevalence, affluence and mean intensity of mites in sexual geckos was significantly higher than in asexuals sharing the same habitat.

In 2011, researchers used the microscopic roundworm Caenorhabditis elegans every bit a host and the pathogenic bacteria Serratia marcescens to generate a host-parasite coevolutionary organisation in a controlled environment, allowing them to conduct more than 70 development experiments testing the Ruby Queen Hypothesis. They genetically manipulated the mating organisation of C. elegans, causing populations to mate either sexually, by cocky-fertilization, or a mixture of both within the aforementioned population. And then they exposed those populations to the S. marcescens parasite. Information technology was constitute that the cocky-fertilizing populations of C. elegans were chop-chop driven extinct by the coevolving parasites while sex allowed populations to keep stride with their parasites, a result consequent with the Red Queen Hypothesis.[23] [24] In natural populations of C. elegans, self-fertilization is the predominant mode of reproduction, just infrequent out-crossing events occur at a charge per unit of about 1%.[25]

Critics of the Red Queen hypothesis question whether the constantly changing surroundings of hosts and parasites is sufficiently mutual to explain the development of sex. In particular, Otto and Nuismer [26] presented results showing that species interactions (due east.g. host vs parasite interactions) typically select against sex. They concluded that, although the Ruby-red Queen hypothesis favors sexual practice under certain circumstances, it solitary does not account for the ubiquity of sex activity. Otto and Gerstein [27] further stated that "it seems doubtful to us that strong pick per factor is sufficiently commonplace for the Red Queen hypothesis to explicate the ubiquity of sex activity". Parker[28] reviewed numerous genetic studies on plant illness resistance and failed to uncover a single case consistent with the assumptions of the Red Queen hypothesis.

Disadvantages of sex and sexual reproduction [edit]

The paradox of the existence of sexual reproduction is that though it is ubiquitous in multicellular organisms, there are ostensibly many inherent disadvantages to reproducing sexually when weighed against the relative advantages of alternative forms of reproduction, such every bit asexual reproduction. Thus, considering sexual reproduction abounds in complex multicellular life, there must be some significant benefit(s) to sex and sexual reproduction that compensates for these cardinal disadvantages.

Population expansion price of sex [edit]

Among the most limiting disadvantages to the evolution of sexual reproduction by natural selection is that an asexual population can abound much more rapidly than a sexual ane with each generation.

For instance, assume that the entire population of some theoretical species has 100 total organisms consisting of ii sexes (i.e. males and females), with 50:l male-to-female representation, and that only the females of this species tin can bear offspring. If all capable members of this population procreated once, a total of 50 offspring would be produced (the F1 generation). Contrast this outcome with an asexual species, in which each and every member of an equally sized 100-organism population is capable of bearing immature. If all capable members of this asexual population procreated one time, a total of 100 offspring would be produced – twice as many equally produced by the sexual population in a single generation.

This diagram illustrates the ii-fold cost of sex activity. If each individual were to contribute to the same number of offspring (2), (a) the sexual population remains the same size each generation, where the (b) asexual population doubles in size each generation.

This idea is sometimes referred to as the 2-fold cost of sexual reproduction. It was first described mathematically by John Maynard Smith.[29] [ page needed ] In his manuscript, Smith further speculated on the bear on of an asexual mutant arising in a sexual population, which suppresses meiosis and allows eggs to develop into offspring genetically identical to the mother by mitotic division.[30] [ page needed ] The mutant-asexual lineage would double its representation in the population each generation, all else existence equal.

Technically the problem above is not i of sexual reproduction but of having a subset of organisms incapable of bearing offspring. Indeed, some multicellular organisms (isogamous) engage in sexual reproduction but all members of the species are capable of bearing offspring.[31] [ page needed ] The two-fold reproductive disadvantage assumes that males contribute only genes to their offspring and sexual females waste half their reproductive potential on sons.[30] [ page needed ] Thus, in this conception, the primary cost of sexual activity is that males and females must successfully copulate, which near always involves expending free energy to come together through time and infinite. Asexual organisms need not expend the energy necessary to observe a mate.

Selfish cytoplasmic genes [edit]

Sexual reproduction implies that chromosomes and alleles segregate and recombine in every generation, only not all genes are transmitted together to the offspring.[30] [ page needed ] At that place is a take a chance of spreading mutants that cause unfair manual at the expense of their non-mutant colleagues. These mutations are referred to as "selfish" because they promote their own spread at the cost of culling alleles or of the host organism; they include nuclear meiotic drivers and selfish cytoplasmic genes.[30] [ page needed ] Meiotic drivers are genes that distort meiosis to produce gametes containing themselves more than the 50% of the fourth dimension expected past chance. A selfish cytoplasmic gene is a gene located in an organelle, plasmid or intracellular parasite that modifies reproduction to cause its own increase at the expense of the jail cell or organism that carries it.[30] [ page needed ]

Genetic heritability price of sex [edit]

A sexually reproducing organism only passes on ~l% of its own genetic material to each L2 offspring. This is a consequence of the fact that gametes from sexually reproducing species are haploid. Again, however, this is not applicative to all sexual organisms. There are numerous species which are sexual but exercise not have a genetic-loss trouble because they exercise not produce males or females. Yeast, for example, are isogamous sexual organisms which take two mating types which fuse and recombine their haploid genomes. Both sexes reproduce during the haploid and diploid stages of their life bike and have a 100% chance of passing their genes into their offspring.[31] [ page needed ]

Some species avoid the 50% price of sexual reproduction, although they have "sex" (in the sense of genetic recombination). In these species (due east.g., bacteria, ciliates, dinoflagellates and diatoms), "sex" and reproduction occurs separately.[32] [33]

DNA repair and complementation [edit]

As discussed in the before function of this article, sexual reproduction is conventionally explained as an adaptation for producing genetic variation through allelic recombination. Every bit best-selling above, however, serious issues with this caption accept led many biologists to conclude that the benefit of sex is a major unsolved trouble in evolutionary biology.

An culling "informational" approach to this problem has led to the view that the two cardinal aspects of sexual activity, genetic recombination and outcrossing, are adaptive responses to the two major sources of "noise" in transmitting genetic information. Genetic racket can occur as either concrete damage to the genome (e.g. chemically altered bases of Deoxyribonucleic acid or breaks in the chromosome) or replication errors (mutations).[34] [35] [36] This alternative view is referred to as the repair and complementation hypothesis, to distinguish it from the traditional variation hypothesis.

The repair and complementation hypothesis assumes that genetic recombination is fundamentally a DNA repair process, and that when it occurs during meiosis it is an adaptation for repairing the genomic Deoxyribonucleic acid which is passed on to progeny. Recombinational repair is the merely repair process known which can accurately remove double-strand damages in Deoxyribonucleic acid, and such amercement are both mutual in nature and ordinarily lethal if not repaired. For instance, double-strand breaks in DNA occur about 50 times per cell cycle in man cells (see naturally occurring Deoxyribonucleic acid damage). Recombinational repair is prevalent from the simplest viruses to the most complex multicellular eukaryotes. It is constructive confronting many different types of genomic damage, and in particular is highly efficient at overcoming double-strand amercement. Studies of the mechanism of meiotic recombination indicate that meiosis is an adaptation for repairing Dna.[37] These considerations course the basis for the first part of the repair and complementation hypothesis.

In some lines of descent from the earliest organisms, the diploid stage of the sexual cycle, which was at starting time transient, became the predominant stage, considering it allowed complementation — the masking of deleterious recessive mutations (i.e. hybrid vigor or heterosis). Outcrossing, the second fundamental aspect of sex, is maintained by the advantage of masking mutations and the disadvantage of inbreeding (mating with a close relative) which allows expression of recessive mutations (commonly observed every bit inbreeding depression). This is in accord with Charles Darwin,[38] who concluded that the adaptive advantage of sex is hybrid vigor; or as he put information technology, "the offspring of two individuals, peculiarly if their progenitors take been subjected to very different conditions, have a great advantage in height, weight, constitutional vigor and fertility over the cocky fertilised offspring from either one of the same parents."

However, outcrossing may be abandoned in favor of parthenogenesis or selfing (which retain the reward of meiotic recombinational repair) under conditions in which the costs of mating are very high. For instance, costs of mating are high when individuals are rare in a geographic expanse, such as when at that place has been a forest burn and the individuals inbound the burned surface area are the initial ones to go far. At such times mates are difficult to detect, and this favors parthenogenic species.

In the view of the repair and complementation hypothesis, the removal of DNA damage by recombinational repair produces a new, less deleterious form of advisory dissonance, allelic recombination, as a by-product. This lesser informational noise generates genetic variation, viewed by some as the major effect of sex activity, as discussed in the before parts of this article.

Deleterious mutation clearance [edit]

Mutations can have many different furnishings upon an organism. Information technology is generally believed that the majority of non-neutral mutations are deleterious, which means that they volition crusade a decrease in the organism's overall fettle.[39] [ page range too broad ] If a mutation has a deleterious consequence, it will then commonly exist removed from the population past the process of natural option. Sexual reproduction is believed to be more efficient than asexual reproduction in removing those mutations from the genome.[40]

In that location are two principal hypotheses which explicate how sex activity may deed to remove deleterious genes from the genome.

Evading harmful mutation build-upwards [edit]

While DNA is able to recombine to modify alleles, Dna is likewise susceptible to mutations inside the sequence that can impact an organism in a negative manner. Asexual organisms practice non have the ability to recombine their genetic information to class new and differing alleles. Once a mutation occurs in the Dna or other genetic conveying sequence, there is no way for the mutation to be removed from the population until another mutation occurs that ultimately deletes the primary mutation. This is rare among organisms.

Hermann Joseph Muller introduced the thought that mutations build up in asexual reproducing organisms. Muller described this occurrence by comparison the mutations that accumulate as a ratchet. Each mutation that arises in asexually reproducing organisms turns the ratchet in one case. The ratchet is unable to be rotated backwards, only forrard. The next mutation that occurs turns the ratchet again. Boosted mutations in a population continually turn the ratchet and the mutations, more often than not deleterious, continually accrue without recombination.[41] These mutations are passed onto the next generation considering the offspring are exact genetic clones of their parents. The genetic load of organisms and their populations will increment due to the improver of multiple deleterious mutations and decrease the overall reproductive success and fitness.

For sexually reproducing populations, studies have shown that single-celled bottlenecks are benign for resisting mutation build-up[ citation needed ]. Passaging a population through a unmarried-celled bottleneck involves the fertilization effect occurring with haploid sets of DNA, forming one fertilized prison cell. For instance, humans undergo a single-celled bottleneck in that the haploid sperm fertilizes the haploid egg, forming the diploid zygote, which is unicellular. This passage through a single cell is beneficial in that it lowers the hazard of mutations from being passed on through multiple individuals. Instead, the mutation is merely passed onto 1 individual.[42] Further studies using Dictyostelium discoideum suggest that this unicellular initial stage is important for resisting mutations due to the importance of high relatedness. Highly related individuals are more than closely related, and more clonal, whereas less related individuals are less so, increasing the likelihood that an private in a population of low relatedness may have a detrimental mutation. Highly related populations also tend to thrive ameliorate than lowly related considering the toll of sacrificing an private is greatly beginning past the benefit gained by its relatives and in turn, its genes, according to kin choice. The studies with D. discoideum showed that weather condition of high relatedness resisted mutant individuals more effectively than those of depression relatedness, suggesting the importance of loftier relatedness to resist mutations from proliferating.[43]

Removal of deleterious genes [edit]

Diagram illustrating different relationships between numbers of mutations and fitness. Kondrashov's model requires synergistic epistasis, which is represented past the reddish line[44] [45] – each subsequent mutation has a disproportionately large effect on the organism'southward fitness.

This hypothesis was proposed past Alexey Kondrashov, and is sometimes known as the deterministic mutation hypothesis.[40] It assumes that the majority of deleterious mutations are merely slightly deleterious, and affect the individual such that the introduction of each boosted mutation has an increasingly large effect on the fettle of the organism. This human relationship between number of mutations and fettle is known as synergistic epistasis.

By way of analogy, retrieve of a car with several small-scale faults. Each is not sufficient alone to forbid the car from running, but in combination, the faults combine to foreclose the car from performance.

Similarly, an organism may be able to cope with a few defects, merely the presence of many mutations could overwhelm its backup mechanisms.

Kondrashov argues that the slightly deleterious nature of mutations means that the population will tend to exist equanimous of individuals with a small number of mutations. Sexual practice volition act to recombine these genotypes, creating some individuals with fewer deleterious mutations, and some with more than. Because there is a major selective disadvantage to individuals with more mutations, these individuals dice out. In essence, sex compartmentalises the deleterious mutations.

In that location has been much criticism of Kondrashov'due south theory, since it relies on two fundamental restrictive conditions. The first requires that the rate of deleterious mutation should exceed one per genome per generation in order to provide a substantial advantage for sex. While there is some empirical testify for it (for example in Drosophila[46] and E. coli[47]), there is also strong evidence against information technology. Thus, for example, for the sexual species Saccharomyces cerevisiae (yeast) and Neurospora crassa (mucus), the mutation charge per unit per genome per replication are 0.0027 and 0.0030 respectively. For the nematode worm Caenorhabditis elegans, the mutation charge per unit per effective genome per sexual generation is 0.036.[48] Secondly, at that place should be strong interactions amidst loci (synergistic epistasis), a mutation-fettle relation for which there is just limited evidence.[49] Conversely, at that place is also the same amount of bear witness that mutations show no epistasis (purely condiment model) or antagonistic interactions (each boosted mutation has a disproportionally small result).

Other explanations [edit]

Geodakyan's evolutionary theory of sex [edit]

Geodakyan suggested that sexual dimorphism provides a sectionalization of a species' phenotypes into at least two functional partitions: a female sectionalisation that secures beneficial features of the species and a male segmentation that emerged in species with more variable and unpredictable environments. The male sectionalization is suggested to be an "experimental" part of the species that allows the species to expand their ecological niche, and to have culling configurations. This theory underlines the higher variability and higher mortality in males, in comparison to females. This functional sectionalization too explains the higher susceptibility to disease in males, in comparison to females and therefore includes the idea of "protection confronting parasites" as another functionality of male sexual activity. Geodakyan'southward evolutionary theory of sex was adult in Russia in 1960–1980 and was not known to the West till the era of the Net. Trofimova, who analysed psychological sex differences, hypothesised that the male sex might also provide a "redundancy pruning" function.[l]

Speed of evolution [edit]

Ilan Eshel suggested that sex prevents rapid development. He suggests that recombination breaks upwardly favourable gene combinations more ofttimes than it creates them, and sex is maintained because it ensures selection is longer-term than in asexual populations – then the population is less affected by short-term changes.[13] : 85–86 [51] This explanation is not widely accepted, as its assumptions are very restrictive.

It has recently been shown in experiments with Chlamydomonas algae that sex can remove the speed limit[ clarification needed ] on evolution.[52]

An information theoretic analysis using a simplified only useful model shows that in asexual reproduction, the information proceeds per generation of a species is limited to 1 bit per generation, while in sexual reproduction, the information gain is bounded by K {\displaystyle {\sqrt {G}}} , where G {\displaystyle G} is the size of the genome in bits.[53]

Libertine bubble theory [edit]

The evolution of sex can alternatively be described every bit a kind of gene exchange that is independent from reproduction.[54] According to the Thierry Lodé's "libertine bubble theory", sexual practice originated from an archaic cistron transfer process among prebiotic bubbles.[55] [56] The contact among the pre-biotic bubbles could, through simple food or parasitic reactions, promote the transfer of genetic textile from one bubble to another. That interactions between 2 organisms be in balance appear to exist a sufficient condition to brand these interactions evolutionarily efficient, i.e. to select bubbles that tolerate these interactions ("libertine" bubbles) through a blind evolutionary process of self-reinforcing gene correlations and compatibility.[57]

The "libertine chimera theory" proposes that meiotic sex activity evolved in proto-eukaryotes to solve a problem that leaner did not have, namely a big amount of Dna material, occurring in an archaic footstep of proto-cell formation and genetic exchanges. And then that, rather than providing selective advantages through reproduction, sex could be idea of as a series of separate events which combines step-by-step some very weak benefits of recombination, meiosis, gametogenesis and syngamy.[58] Therefore, current sexual species could exist descendants of primitive organisms that practiced more stable exchanges in the long term, while asexual species have emerged, much more than recently in evolutionary history, from the conflict of interest resulting from anisogamy.[ clarification needed ]

Parasites and Muller'south ratchet

R. Stephen Howard and Curtis Lively were the offset to suggest that the combined effects of parasitism and mutation accumulation tin lead to an increased advantage to sex activity under weather condition not otherwise predicted (Nature, 1994). Using computer simulations, they showed that when the two mechanisms act simultaneously the advantage to sex over asexual reproduction is larger than for either cistron operating alone.

Origin of sexual reproduction [edit]

Many protists reproduce sexually, every bit do many multicellular plants, animals, and fungi. In the eukaryotic fossil tape, sexual reproduction offset appeared about two.0 billion years ago in the Proterozoic Eon,[59] [60] although a later engagement, ane.2 billion years ago, has too been presented.[61] [62] Nonetheless, all sexually reproducing eukaryotic organisms likely derive from a single-celled mutual antecedent.[1] [63] [55] It is likely that the development of sex was an integral part of the development of the offset eukaryotic cell.[64] [65] There are a few species which have secondarily lost this feature, such as Bdelloidea and some parthenocarpic plants.

Diploidy [edit]

Organisms demand to replicate their genetic cloth in an efficient and reliable manner. The necessity to repair genetic damage is one of the leading theories explaining the origin of sexual reproduction. Diploid individuals tin repair a damaged department of their DNA via homologous recombination, since there are two copies of the gene in the cell and if i re-create is damaged, the other re-create is unlikely to be damaged at the aforementioned site.

A harmful mutation in a haploid individual, on the other manus, is more probable to become fixed (i.due east. permanent), since any Deoxyribonucleic acid repair mechanism would have no source from which to recover the original undamaged sequence.[34] The most primitive form of sex may have been ane organism with damaged Deoxyribonucleic acid replicating an undamaged strand from a similar organism in order to repair itself.[66]

Meiosis [edit]

If, every bit testify indicates, sexual reproduction arose very early on in eukaryotic development, the essential features of meiosis may accept already been present in the prokaryotic ancestors of eukaryotes.[63] [67] In extant organisms, proteins with cardinal functions in meiosis are similar to fundamental proteins in natural transformation in bacteria and Dna transfer in archaea.[67] [68] For example, recA recombinase, that catalyses the key functions of DNA homology search and strand exchange in the bacterial sexual procedure of transformation, has orthologs in eukaryotes that perform similar functions in meiotic recombination[67] (encounter Wikipedia manufactures RecA, RAD51 and DMC1).

Natural transformation in bacteria, DNA transfer in archaea, and meiosis in eukaryotic microorganisms are induced by stressful circumstances such as overcrowding, resource depletion, and DNA damaging weather condition.[57] [67] [68] This suggests that these sexual processes are adaptations for dealing with stress, specially stress that causes Deoxyribonucleic acid damage. In bacteria, these stresses induce an altered physiologic state, termed competence, that allows agile take-up of Deoxyribonucleic acid from a donor bacterium and the integration of this Dna into the recipient genome (see Natural competence) allowing recombinational repair of the recipients' damaged DNA.[69]

If environmental stresses leading to Deoxyribonucleic acid damage were a persistent challenge to the survival of early microorganisms, so selection would likely have been continuous through the prokaryote to eukaryote transition,[58] [67] and adaptative adjustments would have followed a class in which bacterial transformation or archaeal Deoxyribonucleic acid transfer naturally gave ascent to sexual reproduction in eukaryotes.

Virus-like RNA-based origin [edit]

Sex activity might also have been present fifty-fifty earlier, in the hypothesized RNA world that preceded Deoxyribonucleic acid cellular life forms.[seventy] One proposed origin of sexual activity in the RNA globe was based on the blazon of sexual interaction that is known to occur in extant single-stranded segmented RNA viruses, such every bit flu virus, and in extant double-stranded segmented RNA viruses such as reovirus.[71]

Exposure to conditions that crusade RNA damage could have led to blockage of replication and expiry of these early RNA life forms. Sex would have allowed re-array of segments between two individuals with damaged RNA, permitting undamaged combinations of RNA segments to come together, thus allowing survival. Such a regeneration phenomenon, known as multiplicity reactivation, occurs in flu virus[72] and reovirus.[73]

Parasitic Deoxyribonucleic acid elements [edit]

Some other theory is that sexual reproduction originated from selfish parasitic genetic elements that commutation genetic textile (that is: copies of their own genome) for their manual and propagation. In some organisms, sexual reproduction has been shown to raise the spread of parasitic genetic elements (due east.g. yeast, filamentous fungi).[74]

Bacterial conjugation is a course of genetic exchange that some sources describe every bit "sex", but technically is non a form of reproduction, even though it is a form of horizontal cistron transfer. However, it does support the "selfish gene" role theory, since the factor itself is propagated through the F-plasmid.[66]

A similar origin of sexual reproduction is proposed to have evolved in aboriginal haloarchaea as a combination of two independent processes: jumping genes and plasmid swapping.[75]

Partial predation [edit]

A third theory is that sexual practice evolved every bit a form of cannibalism: One primitive organism ate another 1, only instead of completely digesting it, some of the eaten organism'south Dna was incorporated into the DNA of the eater.[66] [64]

Vaccination-like process [edit]

Sexual practice may also be derived from another prokaryotic process. A comprehensive theory chosen "origin of sex as vaccination" proposes that eukaryan sexual practice-as-syngamy (fusion sexual activity) arose from prokaryan unilateral sexual practice-as-infection, when infected hosts began swapping nuclearised genomes containing coevolved, vertically transmitted symbionts that provided protection confronting horizontal superinfection by other, more than virulent symbionts.

Consequently, sex-as-meiosis (fission sex) would evolve as a host strategy for uncoupling from (and thereby render impotent) the acquired symbiotic/parasitic genes.[76]

Mechanistic origin of sexual reproduction [edit]

While theories positing fettle benefits that led to the origin of sex are often problematic,[ citation needed ] several theories addressing the emergence of the mechanisms of sexual reproduction accept been proposed.

Viral eukaryogenesis [edit]

The viral eukaryogenesis (VE) theory proposes that eukaryotic cells arose from a combination of a lysogenic virus, an archaean, and a bacterium. This model suggests that the nucleus originated when the lysogenic virus incorporated genetic cloth from the archaean and the bacterium and took over the part of data storage for the constructing. The archaeal host transferred much of its functional genome to the virus during the evolution of cytoplasm, but retained the part of factor translation and general metabolism. The bacterium transferred well-nigh of its functional genome to the virus equally it transitioned into a mitochondrion.[77]

For these transformations to pb to the eukaryotic cell cycle, the VE hypothesis specifies a pox-like virus as the lysogenic virus. A pox-like virus is a likely ancestor because of its key similarities with eukaryotic nuclei. These include a double stranded DNA genome, a linear chromosome with short telomeric repeats, a complex membrane bound capsid, the power to produce capped mRNA, and the power to export the capped mRNA across the viral membrane into the cytoplasm. The presence of a lysogenic pox-similar virus antecedent explains the evolution of meiotic sectionalisation, an essential component of sexual reproduction.[78]

Meiotic partitioning in the VE hypothesis arose because of the evolutionary pressures placed on the lysogenic virus as a result of its inability to enter into the lytic cycle. This selective pressure resulted in the development of processes allowing the viruses to spread horizontally throughout the population. The outcome of this selection was prison cell-to-cell fusion. (This is distinct from the conjugation methods used by bacterial plasmids under evolutionary pressure, with important consequences.)[77] The possibility of this kind of fusion is supported by the presence of fusion proteins in the envelopes of the pox viruses that allow them to fuse with host membranes. These proteins could have been transferred to the cell membrane during viral reproduction, enabling cell-to-cell fusion between the virus host and an uninfected cell. The theory proposes meiosis originated from the fusion between two cells infected with related only unlike viruses which recognised each other as uninfected. Afterward the fusion of the two cells, incompatibilities betwixt the two viruses result in a meiotic-like jail cell partitioning.[78]

The two viruses established in the cell would initiate replication in response to signals from the host cell. A mitosis-like prison cell cycle would keep until the viral membranes dissolved, at which signal linear chromosomes would be bound together with centromeres. The homologous nature of the two viral centromeres would incite the grouping of both sets into tetrads. It is speculated that this grouping may exist the origin of crossing over, characteristic of the start division in modern meiosis. The partitioning apparatus of the mitotic-like cell cycle the cells used to replicate independently would then pull each set of chromosomes to one side of the jail cell, however spring by centromeres. These centromeres would prevent their replication in subsequent division, resulting in 4 daughter cells with one copy of one of the two original pox-similar viruses. The procedure resulting from combination of 2 similar pox viruses within the same host closely mimics meiosis.[78]

Neomuran revolution [edit]

An alternative theory, proposed by Thomas Condescending-Smith, was labeled the Neomuran revolution. The designation "Neomuran revolution" refers to the appearances of the mutual ancestors of eukaryotes and archaea. Cavalier-Smith proposes that the commencement neomurans emerged 850 million years ago. Other molecular biologists presume that this grouping appeared much earlier, merely Condescending-Smith dismisses these claims because they are based on the "theoretically and empirically" unsound model of molecular clocks. Cavalier-Smith'south theory of the Neomuran revolution has implications for the evolutionary history of the cellular machinery for recombination and sex. It suggests that this machinery evolved in two distinct bouts separated by a long period of stasis; first the advent of recombination mechanism in a bacterial ancestor which was maintained for 3 Gy,[ description needed ] until the neomuran revolution when the mechanics were adapted to the presence of nucleosomes. The archaeal products of the revolution maintained recombination mechanism that was essentially bacterial, whereas the eukaryotic products broke with this bacterial continuity. They introduced cell fusion and ploidy cycles into cell life histories. Cavalier-Smith argues that both bouts of mechanical evolution were motivated by similar selective forces: the need for accurate DNA replication without loss of viability.[79]

Questions [edit]

Some questions biologists have attempted to answer include:

  • Why does sexual reproduction be, if in many organisms it has a 50% toll (fitness disadvantage) in relation to asexual reproduction?[32]
  • Did mating types (types of gametes, according to their compatibility) arise as a outcome of anisogamy (gamete dimorphism), or did mating types evolve before anisogamy?[80] [81]
  • Why do most sexual organisms apply a binary mating arrangement? Grouping itself offers a survival advantage. A binary recognition based system is the near simple and constructive method in maintaining species grouping.[82]
  • Why do some organisms have gamete dimorphism?

References [edit]

  1. ^ a b Letunic, I; Bork, P (2006). "Interactive Tree of Life". Retrieved 23 July 2011.
  2. ^ mLetunic, I; Bork, P (2007). "Interactive Tree of Life (iTOL): An online tool for phylogenetic tree display and annotation" (PDF). Bioinformatics. 23 (1): 127–8. doi:ten.1093/bioinformatics/btl529. PMID 17050570.
  3. ^ Letunic, I; Bork, P (2011). "Interactive Tree of Life v2: Online annotation and brandish of phylogenetic trees made easy" (PDF). Nucleic Acids Inquiry. 39 (Spider web Server issue): W475–8. doi:10.1093/nar/gkr201. PMC3125724. PMID 21470960.
  4. ^ Otto, Sarah (2014). "Sexual Reproduction and the Evolution of Sex activity". Scitable . Retrieved 28 February 2019.
  5. ^ Goodenough, U.; Heitman, J. (1 March 2014). "Origins of Eukaryotic Sexual Reproduction". Cold Spring Harbor Perspectives in Biological science. 6 (3): a016154. doi:10.1101/cshperspect.a016154. ISSN 1943-0264. PMC3949356. PMID 24591519.
  6. ^ Darwin, Erasmus (1800). Phytologia …. Dublin, Ireland: P. Byrne. p. 104. From p. 104: "Every bit the progeny by lateral generation [i.e., vegetative (asexual) reproduction] and then exactly resembles the parent stock, it follows, that though whatever new variety, or improvement, may exist thus continued for a century or two, as in grafted fruit-trees, withal that no new multifariousness or improvements can be obtained by this mode of generation; … " "But from the sexual, or amatorial, generation of plants new varieties, or improvements, are oftentimes obtained; as many of the immature plants from seeds are dissimilar to the parent, and some of them supererior to the parent in the qualities we wish to possess; … " " … another advantage occurs from sexual generation, which is the production of new species of plants, or mules, … "
  7. ^ English translation: Weismann, August (1889). Poulton, Edward B.; Schönland, Selmar; Shipley, Arthur E. (eds.). Essays Upon Heredity and Kindred Biological Problems. Oxford, England: Clarendon Press. pp. 252–332. Ch. 5: The Significance of Sexual Reproduction in the Theory of Natural Choice (1886)
    • Weismann, Aug. (1885) "Dice Bedeutung der sexuellen Fortpflanzung für die Selektions-Theorie" [The significance of sexual reproduction in the theory of natural selection] Stilling, J. (ed.) Tageblatt der 58. Versammlung Deutscher Naturforscher und Aerzte in Strassburg [Daily News of the 58th Conference of German Natural Scientists and Physicians in Strassburg] (in German) Strassburg, Federal republic of germany: Yard. Fischbach pp. 42-56.
    • Revised and expanded in: Weismann, August (1886). Die Bedeutung der sexuellen Fortpflanzung für die Selektions-Theorie (in German). Jena, Germany: Gustav Fischer.
  8. ^ Darwin, Charles (1876). The Effects of Cross and Cocky Fertilisation in the Vegetable Kingdom. London, England: John Murray. p. 462.
  9. ^ Crow J.F. (1994). Advantages of Sexual Reproduction, Dev. Gen., vol.15, pp. 205-213.
  10. ^ Goldstein, R Northward (2010). 36 Arguments for the Existence of God: A Piece of work of Fiction. Pantheon. ISBN978-0-307-37818-7.
  11. ^ Heng HH; Heng, Henry H.Q. (2007). "Elimination of altered karyotypes by sexual reproduction preserves species identity". Genome. 50 (5): 517–524. doi:10.1139/g07-039. PMID 17612621.
  12. ^ Gorelick R, Heng HH; Heng (2011). "Sex reduces genetic variation: a multidisciplinary review". Evolution. 65 (four): 1088–1098. doi:ten.1111/j.1558-5646.2010.01173.x. PMID 21091466.
  13. ^ a b c Birdsell, JA; Wills, C (2003). The evolutionary origin and maintenance of sexual recombination: A review of contemporary models. Evolutionary Biological science. Vol. 33. pp. 27–137. doi:10.1007/978-1-4757-5190-1_2. ISBN978-1-4419-3385-0.
  14. ^ Matt Ridley 1995 The Red Queen: Sexual practice and the Development of Human Nature 1995 Penguin.
  15. ^ MacIntyre, Ross J.; Clegg, Michael, T (Eds.), Springer. Hardcover ISBN 978-0306472619, ISBN 0306472619 Softcover ISBN 978-1-4419-3385-0.
  16. ^ Van Valen, 50. (1973). "A New Evolutionary Law". Evolutionary Theory. 1: 1–30.
  17. ^ Hamilton, W. D.; Axelrod, R.; Tanese, R. (1990). "Sexual reproduction equally an adaptation to resist parasites". Proceedings of the National Academy of Sciences. 87 (9): 3566–3573. Bibcode:1990PNAS...87.3566H. doi:ten.1073/pnas.87.9.3566. PMC53943. PMID 2185476.
  18. ^ Kuma, One thousand.; Iwabe, N.; Miyata, T. (1995). "Functional constraints against variations on molecules from the tissue-level - slowly evolving brain-specific genes demonstrated past protein-kinase and immunoglobulin supergene families". Molecular Biology and Evolution. 12 (1): 123–130. doi:x.1093/oxfordjournals.molbev.a040181. PMID 7877487.
  19. ^ Wolfe KH, Sharp PM; Sharp (1993). "Mammalian factor evolution - nucleotide-sequence divergence betwixt mouse and rat". Journal of Molecular Development. 37 (four): 441–456. Bibcode:1993JMolE..37..441W. doi:ten.1007/BF00178874. PMID 8308912. S2CID 10437152.
  20. ^ Jokela, Jukka; Dybdahl, Mark; Lively, Curtis (2009). "The Maintenance of Sex, Clonal Dynamics, and Host-Parasite Coevolution in a Mixed Population of Sexual and Asexual Snails". The American Naturalist. 174 (s1): S43–53. doi:ten.1086/599080. JSTOR 10.1086/599080. PMID 19441961. S2CID 6797643.
  21. ^ "Parasites May Have Had Office In Development Of Sex". Scientific discipline Daily. 31 July 2009. Retrieved 19 September 2011.
  22. ^ Hanley KA; Fisher RN; Example TJ (1995). "Lower mite infestations in an asexual gecko compared with its sexual ancestors". Evolution. 49 (3): 418–426. doi:x.2307/2410266. JSTOR 2410266. PMID 28565091.
  23. ^ Morran, Levi T.; Schmidt, Olivia G.; Gelarden, Ian A.; Parrish Rc, Raymond C.; Lively, Curtis M. (2011). "Running with the Red Queen: Host-Parasite Coevolution Selects for Biparental Sexual practice". Science. 333 (6039): 216–218. Bibcode:2011Sci...333..216M. doi:ten.1126/science.1206360. PMC3402160. PMID 21737739.
  24. ^ "Sex -- As We Know It -- Works Thanks to Ever-Evolving Host-Parasite Relationships, Biologists Discover". Science Daily. 9 July 2011. Retrieved nineteen September 2011.
  25. ^ Barrière A, Félix MA (July 2005). "High local genetic diverseness and low outcrossing rate in Caenorhabditis elegans natural populations". Curr. Biol. 15 (13): 1176–84. arXiv:q-bio/0508003. Bibcode:2005q.bio.....8003B. doi:10.1016/j.cub.2005.06.022. PMID 16005289. S2CID 2229622.
  26. ^ Otto SP, Nuismer SL; Nuismer (2004). "Species interactions and the development of sex". Science. 304 (5673): 1018–1020. Bibcode:2004Sci...304.1018O. doi:ten.1126/science.1094072. PMID 15143283. S2CID 8599387.
  27. ^ Otto SP, Gerstein AC; Gerstein (Baronial 2006). "Why take sex? The population genetics of sex and recombination". Biochemical Society Transactions. 34 (Pt 4): 519–22. doi:10.1042/BST0340519. PMID 16856849.
  28. ^ Parker MA (1994). "Pathogens and sex in plants". Evolutionary Ecology. eight (5): 560–584. doi:x.1007/BF01238258. S2CID 31756267.
  29. ^ Smith, J. Maynard (1978). The Evolution of Sex . Cambridge Academy Printing. ISBN9780521293020.
  30. ^ a b c d e Stearns, South. C. (2005). Evolution : an introduction. Hoekstra, Rolf F. (2d ed.). Oxford [England]: Oxford Academy Press. ISBN978-0199255634. OCLC 56964580.
  31. ^ a b Hoekstra, Rolf F. (1987). "The Development of Sexes". In Stearns, Stephen C. (ed.). The Development of Sex and its Consequences. Springer Basel AG. ISBN9783034862738.
  32. ^ a b Ridley, Mark (2003). Evolution (third ed.). Wiley. p. 314. ISBN9781405103459.
  33. ^ Beukeboom, L. & Perrin, N. (2014). The Evolution of Sexual activity Determination. Oxford University Printing, p. 5–half-dozen [1]. Online resources, [two].
  34. ^ a b Bernstein H; Byerly HC; Hopf FA; Michod RE (1984). "Origin of sex". J. Theor. Biol. 110 (iii): 323–51. Bibcode:1984JThBi.110..323B. doi:10.1016/S0022-5193(84)80178-2. PMID 6209512.
  35. ^ Bernstein H; Byerly HC; Hopf FA; Michod RE (1985). "Genetic damage, mutation, and the development of sex activity". Science. 229 (4719): 1277–81. Bibcode:1985Sci...229.1277B. doi:10.1126/science.3898363. PMID 3898363.
  36. ^ Bernstein H; Hopf FA; Michod RE (1987). The Molecular Footing of the Evolution of Sexual activity. Adv. Genet. Advances in Genetics. Vol. 24. pp. 323–70. doi:10.1016/S0065-2660(08)60012-7. ISBN9780120176243. PMID 3324702.
  37. ^ Cox MM (2001). "Historical overview: searching for replication help in all of the rec places". Proc. Natl. Acad. Sci. U.Due south.A. 98 (15): 8173–80. Bibcode:2001PNAS...98.8173C. doi:10.1073/pnas.131004998. PMC37418. PMID 11459950.
  38. ^ Darwin CR (1876). The effects of cross and cocky fertilisation in the vegetable kingdom. London: John Murray. [3] see folio 462
  39. ^ Griffiths et al. 1999. Factor mutations, p197-234, in Mod Genetic Analysis, New York, W.H. Freeman and Company.
  40. ^ a b Kondrashov, A. Due south. (1988). "Deleterious mutations and the evolution of sexual reproduction". Nature. 336 (6198): 435–440. Bibcode:1988Natur.336..435K. doi:10.1038/336435a0. PMID 3057385. S2CID 4233528.
  41. ^ Muller, H.J. (1964). "The Relation of Recombination to Mutational Accelerate". Mutation Research. 1: ii–9. doi:10.1016/0027-5107(64)90047-8. PMID 14195748.
  42. ^ Niklas, Karl J. (i January 2014). "The evolutionary-developmental origins of multicellularity". American Periodical of Botany. 101 (1): 6–25. doi:10.3732/ajb.1300314. ISSN 0002-9122. PMID 24363320.
  43. ^ Kuzdzal-Fick, Jennie J.; Flim-flam, Sara A.; Strassmann, Joan Due east.; Queller, David C. (16 December 2011). "High Relatedness Is Necessary and Sufficient to Maintain Multicellularity in Dictyostelium". Science. 334 (6062): 1548–1551. Bibcode:2011Sci...334.1548K. doi:10.1126/science.1213272. ISSN 0036-8075. PMID 22174251. S2CID 206537272.
  44. ^ Ridley M (2004) Evolution, 3rd edition. Blackwell Publishing.
  45. ^ Charlesworth B, Charlesworth D (2010) Elements of Evolutionary Genetics. Roberts and Company Publishers.
  46. ^ Whitlock, M. C.; Bourguet, D. (2000). "Factors affecting the genetic load in Drosophila: synergistic epistasis and correlations amid fettle components" (PDF). Evolution. 54 (v): 1654–1660. doi:10.1554/0014-3820(2000)054[1654:fatgli]2.0.co;ii. PMID 11108592. S2CID 198153635.
  47. ^ Elena, S. F.; Lenski, R. E. (1997). "Test of synergistic interactions among deleterious mutations in bacteria". Nature. 390 (6658): 395–398. Bibcode:1997Natur.390..395E. doi:10.1038/37108. PMID 9389477. S2CID 205025450.
  48. ^ Drake JW; Charlesworth B; Charlesworth D; Crow JF (April 1998). "Rates of spontaneous mutation". Genetics. 148 (4): 1667–86. doi:10.1093/genetics/148.4.1667. PMC1460098. PMID 9560386.
  49. ^ Sohail, One thousand; Vakhrusheva, OA; Sul, JH; Pulit, SL; Francioli, LC; van den Berg, LH; Veldink, JH; de Bakker, PIW; Bazykin, GA; Kondrashov, AS; Sunyaev, SR (2017). "Negative choice in humans and fruit flies involves synergistic epistasis". Scientific discipline. 356 (6337): 539–542. Bibcode:2017Sci...356..539S. doi:10.1126/science.aah5238. PMC6200135. PMID 28473589.
  50. ^ Trofimova, I. (2015). "Do psychological sex differences reflect evolutionary bi-sexual sectionalisation?". American Journal of Psychology. 128 (iv): 485–514. doi:10.5406/amerjpsyc.128.four.0485. PMID 26721176.
  51. ^ Eshel, I.; Feldman, MW (May 1970). "On the evolutionary effect of recombination". Theoretical Population Biological science. ane (ane): 88–100. doi:ten.1016/0040-5809(lxx)90043-two. PMID 5527627.
  52. ^ Colegrave, Due north. (2002). "Sex releases the speed limit on evolution". Nature. 420 (6916): 664–666. Bibcode:2002Natur.420..664C. doi:ten.1038/nature01191. hdl:1842/692. PMID 12478292. S2CID 4382757.
  53. ^ David MacKay (2003). Data Theory, Inference, and Learning Algorithms (PDF). Cambridge: Cambridge University Press. pp. 269–280.
  54. ^ Lesbarrères D (2011). "Sex activity or no sex, reproduction is not the question". BioEssays. 33 (11): 818. doi:ten.1002/bies.201100105. PMID 22009640. S2CID 46112804.
  55. ^ a b Lodé, T (2011). "Sex activity is not a solution for reproduction: the libertine bubble theory". BioEssays. 33 (half-dozen): 419–422. doi:x.1002/bies.201000125. PMID 21472739.
  56. ^ Lodé, T (2011). "The origin of sex was interaction, not reproduction (what'due south sexual practice actually all about), Large Idea". New Scientist. 212 (2837): 30–31. doi:ten.1016/S0262-4079(11)62719-X.
  57. ^ a b Lodé, T (2012). "Sex activity and the origin of genetic exchanges". Trends Evol Biol. 4: e1. doi:ten.4081/eb.2012.e1.
  58. ^ a b Lodé, T (2012). "Have sex or non ? Lessons from bacteria". Sexual Dev. 6 (vi): 325–328. doi:10.1159/000342879. PMID 22986519.
  59. ^ Otto, Sarah P. (2008). "Sexual Reproduction and the Evolution of Sex". Nature . Retrieved i October 2021.
  60. ^ Zimmer, Carl (5 June 2009). "On The Origin Of Sexual Reproduction". Science. 324 (5932): 1254–1256. doi:10.1126/science.324_1254. PMID 19498143. Retrieved one Oct 2021.
  61. ^ Butterfield, Nicholas J. (2000). "Bangiomorpha pubescens northward. gen., n. sp.: implications for the development of sex activity, multicellularity, and the Mesoproterozoic/Neoproterozoic radiation of eukaryotes". Paleobiology. 26 (3): 386. doi:ten.1666/0094-8373(2000)026<0386:BPNGNS>two.0.CO;2. S2CID 36648568. Retrieved 12 April 2021.
  62. ^ Cumming, Vivian (four July 2016). "The Real Reasons Why We Accept Sex". BBC News . Retrieved 12 April 2021.
  63. ^ a b Bernstein H, Bernstein C (2010). "Evolutionary origin of recombination during meiosis". BioScience. 60 (7): 498–505. doi:ten.1525/bio.2010.60.vii.5. S2CID 86663600.
  64. ^ a b Ploompuu, T. (1999). Biosüsteemide mälu teooria [Why the eukaryotic cell retention was needed]. Schola Biotheoretica (in Estonian). Vol. XXV. Tartu: Sulemees. pp. 51–56. ISBN978-9985908150. Abstruse in English bachelor online: [4]
  65. ^ Hörandl Due east, Speijer D (February 2018). "How oxygen gave rise to eukaryotic sexual activity". Proc. Biol. Sci. 285 (1872): 20172706. doi:ten.1098/rspb.2017.2706. PMC5829205. PMID 29436502.
  66. ^ a b c Olivia Judson (2002). Dr. Tatiana's sex communication to all creation. New York: Metropolitan Books. pp. 233–4. ISBN978-0-8050-6331-viii.
  67. ^ a b c d e Bernstein, H., Bernstein, C. Evolutionary origin and adaptive part of meiosis. In "Meiosis", Intech Publ (Carol Bernstein and Harris Bernstein editors), Chapter 3: 41-75 (2013).
  68. ^ a b Bernstein H, Bernstein C. Sexual communication in archaea, the precursor to meiosis. pp. 103-117 in Witzany, Guenther, ed. (2017). Biocommunication of Archaea. doi:x.1007/978-3-319-65536-9. ISBN978-3-319-65535-2. S2CID 26593032.
  69. ^ Michod RE, Wojciechowski MF, Hoelzer MA (1988). "Deoxyribonucleic acid repair and the evolution of transformation in the bacterium Bacillus subtilis". Genetics. 118 (i): 31–39. doi:10.1093/genetics/118.1.31. PMC1203263. PMID 8608929.
  70. ^ Eigen M, Gardiner W, Schuster P, Winkler-Oswatitsch R (April 1981). "The origin of genetic data". Scientific American. 244 (4): 88–92, 96, et passim. Bibcode:1981SciAm.244d..88E. doi:x.1038/scientificamerican0481-88. PMID 6164094.
  71. ^ Bernstein H, Byerly HC, Hopf FA, Michod RE (October 1984). "Origin of sex". Journal of Theoretical Biology. 110 (3): 323–351. Bibcode:1984JThBi.110..323B. doi:ten.1016/S0022-5193(84)80178-2. PMID 6209512.
  72. ^ Barry RD (1961). "The multiplication of influenza virus. 2. Multiplicity reactivation of ultraviolet irradiated virus". Virology. 14 (4): 398–405. doi:ten.1016/0042-6822(61)90330-0. hdl:1885/109240. PMID 13687359.
  73. ^ McClain ME, Spendlove RS (1966). "Multiplicity reactivation of reovirus particles after exposure to ultraviolet light". J Bacteriol. 92 (v): 1422–1429. doi:10.1128/JB.92.5.1422-1429.1966. PMC276440. PMID 5924273.
  74. ^ Hickey D (1982). "Selfish Dna: a sexually-transmitted nuclear parasite". Genetics. 101 (iii–4): 519–531. doi:10.1093/genetics/101.iii-four.519. PMC1201875. PMID 6293914.
  75. ^ DasSarma, Shiladitya (2007). "Extreme Microbes". American Scientist. 95 (3): 224–231. doi:ten.1511/2007.65.224.
  76. ^ Sterrer W (2002). "On the origin of sex as vaccination". Periodical of Theoretical Biological science. 216 (4): 387–396. Bibcode:2002JThBi.216..387S. doi:10.1006/jtbi.2002.3008. PMID 12151256.
  77. ^ a b Bong, PJ (2001). "Viral eukaryogenesis: Was the ancestor of the nucleus a circuitous Deoxyribonucleic acid virus?". Periodical of Molecular Biological science. 53 (3): 251–256. Bibcode:2001JMolE..53..251L. doi:10.1007/s002390010215. PMID 11523012. S2CID 20542871.
  78. ^ a b c Bell, PJ (2006). "Sex and the eukaryotic cell cycle is consistent with a viral ancestry for the eukaryotic nucleus". Periodical of Theoretical Biology. 243 (i): 54–63. Bibcode:2006JThBi.243...54B. doi:10.1016/j.jtbi.2006.05.015. PMID 16846615.
  79. ^ Condescending-Smith, Thomas (2006). "Cell evolution and Earth history: Stasis and revolution". Philosophical Transactions of the Regal Society B: Biological Sciences. 361 (1470): 969–1006. doi:10.1098/rstb.2006.1842. PMC1578732. PMID 16754610.
  80. ^ T. Togashi, P. Cox (Eds.) The Evolution of Anisogamy. Cambridge University Printing, Cambridge; 2011, p. 22-29.
  81. ^ Beukeboom, L. & Perrin, N. (2014). The Evolution of Sexual activity Determination. Oxford University Press, p. 25 [5]. Online resources, [6].
  82. ^ Czárán, T.50.; Hoekstra, R.F. (2006). "Evolution of sexual asymmetry". BMC Evolutionary Biology. four: 34–46. doi:10.1186/1471-2148-4-34. PMC524165. PMID 15383154.

Further reading [edit]

  • Bell, Graham (1982). The masterpiece of nature: the evolution and genetics of sexuality. Berkeley: University of California Press. ISBN978-0-520-04583-v.
  • Bernstein, Carol; Harris Bernstein (1991). Aging, sex, and Deoxyribonucleic acid repair. Boston: Bookish Printing. ISBN978-0-12-092860-six.
  • Hurst, L.D.; J.R. Peck (1996). "Contempo advances in the understanding of the evolution and maintenance of sex". Trends in Ecology and Evolution. 11 (2): 46–52. doi:10.1016/0169-5347(96)81041-10. PMID 21237760.
  • Levin, Bruce R.; Richard E. Michod (1988). The Evolution of sexual activity: an examination of current ideas . Sunderland, Mass: Sinauer Associates. ISBN978-0-87893-459-1.
  • Maynard Smith, John (1978). The evolution of sexual activity. Cambridge, U.k.: Cambridge University Printing. ISBN978-0-521-21887-0.
  • Michod, Richard E. (1995). Eros and evolution: a natural philosophy of sex. Reading, Mass: Addison-Wesley Pub. Co. ISBN978-0-201-40754-ix.
  • "Scientists put sexual practice origin mystery to bed, Wild strawberry research provides evidence on when gender emerges". NBC News . Retrieved 25 November 2008.
  • Ridley, Mark (1993). Development. Oxford: Blackwell Scientific. ISBN978-0-632-03481-9.
  • Ridley, Mark (2000). Mendel's demon: gene justice and the complexity of life. London: Weidenfeld & Nicolson. ISBN978-0-297-64634-1.
  • Ridley, Matt (1995). The Red Queen: sexual practice and the evolution of human nature. New York: Penguin Books. ISBN978-0-14-024548-6.
  • Szathmáry, Eörs; John Maynard Smith (1995). The Major Transitions in Evolution. Oxford: W.H. Freeman Spektrum. ISBN978-0-7167-4525-9.
  • Taylor, Timothy (1996). The prehistory of sex: four one thousand thousand years of human sexual civilisation. New York: Bantam Books. ISBN978-0-553-09694-1.
  • Williams, George (1975). Sex activity and development. Princeton, N.J: Princeton Academy Press. ISBN978-0-691-08147-2.

External links [edit]

  • Why Sex activity is Adept
  • An essay summarising the different theories, dating from around 2001
  • http://www.evolocus.com/Textbooks/Geodakian2012.pdf

Advantages And Disadvantages Of Mutation,

Source: https://en.wikipedia.org/wiki/Evolution_of_sexual_reproduction

Posted by: hunterpubleausing.blogspot.com

0 Response to "Advantages And Disadvantages Of Mutation"

Post a Comment

Subscribe to: Post Comments (Atom)

Iklan Atas Artikel

Iklan Tengah Artikel 1

Iklan Tengah Artikel 2

Iklan Bawah Artikel