scholarly journals Population genetic aspects of deleterious cytoplasmic genomes and their effect on the evolution of sexual reproduction

1992 ◽  
Vol 59 (3) ◽  
pp. 215-225 ◽  
Author(s):  
Ian M. Hastings

SummaryA conflict of interest may arise between intra-cellular genomes and their host cell. The example explicitly investigated is that of a ‘selfish’ mitochondrion which increases its own rate of replication at the cost of reduced metabolic activity which is deleterious to the host cell. The results apply to deleterious cytoplasmic agents in general, such as intracellular parasites. Numerical simulation suggests that selfish mitochondria are able to invade an isogamous sexual population and are capable of reducing its fitness to below “5 % of that prior to their invasion. Their spread is enhanced by decreasing the number of mitotic divisions between meioses, and this may constitute a significant constraint on the evolution of lifecycles. The presence of such deleterious cytoplasmic agents favours a nuclear mutation whose expression prevents cytoplasm from the other gamete entering the zygote at fertilization, resulting in uniparental inheritance of cytoplasm. Such a mutation appears physiologically plausible and can increase in frequency despite its deleterious effect in halving the amount of cytoplasm in the zygote. It is suggested that these were the conditions under which anisogamy evolved. These results have implications for the evolution of sexual reproduction. Standard theory suggests there is no immediate cost of sex, a twofold cost being incurred later as anisogamy evolves. The analysis described here predicts a large, rapid reduction in fitness associated with isogamous sexual reproduction, due to the spread of deleterious cytoplasmic agents with fitness only subsequently rising to a maximum twofold cost as uniparental inheritance of cytoplasm and anisogamy evolve.

2006 ◽  
Vol 2 (4) ◽  
pp. 536-538 ◽  
Author(s):  
Marcel Salathé

Sexual selection is a powerful and ubiquitous force in sexual populations. It has recently been argued that sexual selection can eliminate the twofold cost of sex even with low genomic mutation rates. By means of differential male mating success, deleterious mutations in males become more deleterious than in females, and it has been shown that sexual selection can drastically reduce the mutational load in a sexual population, with or without any form of epistasis. However, any mechanism that claims to maintain sexual reproduction must be able to prevent the fixation of an asexual mutant clone with a twofold fitness advantage. Here, I show that despite very strong sexual selection, the fixation of an asexual mutant cannot be prevented under reasonable genomic mutation rates. Sexual selection can have a strong effect on the average mutational load in a sexual population, but as it cannot prevent the fixation of an asexual mutant, it is unlikely to play a key role on the maintenance of sexual reproduction.


2021 ◽  
Author(s):  
Donal Hickey ◽  
Brian Golding

Abstract BackgroundNatural populations harbor significant levels of genetic variability. Because of this standing genetic variation, the number of possible genotypic combinations is many orders of magnitude greater than the population size. This means that any given population contains only a tiny fraction of all possible genotypic combinations.ResultsWe show that recombination allows a finite population to resample the genotype pool, i.e., the universe of all possible genotypic combinations. Recombination, in combination with natural selection, enables an evolving sexual population to replace existing genotypes with new, higher-fitness genotypic combinations that did not previously exist in the population. Gradually the selected sexual population approaches a state where the optimum genotype is produced by recombination and where it rises to fixation. In contrast to this, an asexual population is limited to selection among existing lower fitness genotypes.ConclusionsThe significance of the result is two-fold. First, it provides an explanation for the ubiquity of sexual reproduction in evolving populations. Secondly, it shows that recombination serves to remove concerns about the cost of natural selection acting on the naturally occurring standing genetic variation. This means that classic population genetics theory is applicable to ecological studies of natural selection acting on standing genetic variation.


Genetics ◽  
1998 ◽  
Vol 150 (2) ◽  
pp. 523-532 ◽  
Author(s):  
Paul E Turner ◽  
Lin Chao

Abstract Sex allows beneficial mutations that occur in separate lineages to be fixed in the same genome. For this reason, the Fisher-Muller model predicts that adaptation to the environment is more rapid in a large sexual population than in an equally large asexual population. Sexual reproduction occurs in populations of the RNA virus φ6 when multiple bacteriophages coinfect the same host cell. Here, we tested the model's predictions by determining whether sex favors more rapid adaptation of φ6 to a bacterial host, Pseudomonas phaseolicola. Replicate populations of φ6 were allowed to evolve in either the presence or absence of sex for 250 generations. All experimental populations showed a significant increase in fitness relative to the ancestor, but sex did not increase the rate of adaptation. Rather, we found that the sexual and asexual treatments also differ because intense intrahost competition between viruses occurs during coinfection. Results showed that the derived sexual viruses were selectively favored only when coinfection is common, indicating that within-host competition detracts from the ability of viruses to exploit the host. Thus, sex was not advantageous because the cost created by intrahost competition was too strong. Our findings indicate that high levels of coinfection exceed an optimum where sex may be beneficial to populations of φ6, and suggest that genetic conflicts can evolve in RNA viruses.


2021 ◽  
Author(s):  
Gilbert Roberts ◽  
Marion Petrie

The evolution and widespread maintenance of sexual reproduction remains a conundrum in biology because asexual reproduction should allow twice the reproductive rate. One hypothesis is that sexual selection lessens the negative impact on fitness of accumulating deleterious mutations. However, for adaptation to occur, there must also be selection for beneficial mutations. Here we show that sexual selection can help explain the evolution and maintenance of sexual reproduction. In our model, females chose males with more beneficial mutations (as opposed to just fewer harmful ones) even when these occurred much more rarely. Sexual selection thereby increased fixation of beneficial mutations which increased the absolute genetic quality of sexual offspring. This increase in fitness relative to asexual offspring adds to the previously postulated effect of reduced mutation load in offsetting the cost of sex. Analysing our simulations reveals that female choice among males raised the fitness of reproducing males above that of females. We found that this effect could overcome the decline in average fitness that occurs when mutation rate increases, allowing an increase in the fixation of beneficial mutations. Sexual selection thereby not only facilitates the evolution of sexual reproduction but maintains sex by leveraging its benefits and driving adaptation.


2019 ◽  
Author(s):  
Vida Ahyong ◽  
Charles A. Berdan ◽  
Daniel K. Nomura ◽  
Matthew D. Welch

AbstractGram-negative bacteria in the order Rickettsiales are obligate intracellular parasites that cause human diseases such typhus and spotted fever. They have evolved a dependence on essential nutrients and metabolites from the host cell as a consequence of extensive genome streamlining. However, it remains largely unknown which nutrients they require and whether their metabolic dependency can be exploited therapeutically. Here, we describe a genetic rewiring of bacterial isoprenoid biosynthetic pathways in the Rickettsiales that has resulted from reductive genome evolution. We further investigated whether the spotted fever groupRickettsiaspeciesRickettsia parkeriscavenges isoprenoid precursors directly from the host. Using targeted mass spectrometry in uninfected and infected cells, we found decreases in host isoprenoid products and concomitant increases in bacterial isoprenoid metabolites. Additionally, we report that bacterial growth is prohibited by inhibition of the host isoprenoid pathway with the statins class of drugs. We show that growth inhibition correlates with changes in bacterial size and shape that mimic those caused by antibiotics that inhibit peptidoglycan biosynthesis, suggesting statins inhibit cell wall synthesis. Altogether, our results describe an Achilles’ heel of obligate intracellular pathogens that can be exploited with host-targeted therapeutics that interfere with metabolic pathways required for bacterial growth.ImportanceObligate intracellular parasites, which include viruses as well as certain bacteria and eukaryotes, extract essential nutrients and metabolites from their host cell. As a result, these pathogens have often lost essential biosynthetic pathways and are metabolically dependent on the host. In this study, we describe a metabolic dependency of the bacterial pathogenRickettsia parkerion host isoprenoid molecules that are used in the biosynthesis of downstream products including cholesterol, steroid hormones, and heme. Bacteria make products from isoprenoids such as an essential lipid carrier for making the bacterial cell wall. We show that bacterial metabolic dependency can represent an Achilles’ heel, and that inhibiting host isoprenoid biosynthesis with the FDA-approved statin class of drugs inhibits bacterial growth by interfering with the integrity of the cell wall. This work highlights a potential to treat infections by obligate intracellular pathogens through inhibition of host biosynthetic pathways that are susceptible to parasitism.


2014 ◽  
Vol 21 (1) ◽  
pp. 187-199 ◽  
Author(s):  
Y. Michel

Abstract. Several consistency diagnostics have been proposed to evaluate variational assimilation schemes. The "Bennett-Talagrand" criterion in particular shows that the cost-function at the minimum should be close to half the number of assimilated observations when statistics are correctly specified. It has been further shown that sub-parts of the cost function also had statistical expectations that could be expressed as traces of large matrices, and that this could be exploited for variance tuning and hypothesis testing. The aim of this work is to extend those results using standard theory of quadratic forms in random variables. The first step is to express the sub-parts of the cost function as quadratic forms in the innovation vector. Then, it is possible to derive expressions for the statistical expectations, variances and cross-covariances (whether the statistics are correctly specified or not). As a consequence it is proven in particular that, in a perfect system, the values of the background and observation parts of the cost function at the minimum are positively correlated. These results are illustrated in a simplified variational scheme in a one-dimensional context. These expressions involve the computation of the trace of large matrices that are generally unavailable in variational formulations of the assimilation problem. It is shown that the randomization algorithm proposed in the literature can be extended to cover these computations, yet at the price of additional minimizations. This is shown to provide estimations of background and observation errors that improve forecasts of the operational ARPEGE model.


2007 ◽  
Vol 274 (1615) ◽  
pp. 1301-1307 ◽  
Author(s):  
Mohammad A Mandegar ◽  
Sarah P Otto

The ubiquity of sexual reproduction despite its cost has lead to an extensive body of research on the evolution and maintenance of sexual reproduction. Previous work has suggested that sexual reproduction can substantially speed up the rate of adaptation in diploid populations, because sexual populations are able to produce the fittest homozygous genotype by segregation and mating of heterozygous individuals. In contrast, asexual populations must wait for two rare mutational events, one producing a heterozygous carrier and the second converting a heterozygous to a homozygous carrier, before a beneficial mutation can become fixed. By avoiding this additional waiting time, it was shown that the benefits of segregation could overcome a twofold cost of sex. This previous result ignores mitotic recombination (MR), however. Here, we show that MR significantly hastens the spread of beneficial mutations in asexual populations. Indeed, given empirical data on MR, we find that adaptation in asexual populations proceeds as fast as that in sexual populations, especially when beneficial alleles are partially recessive. We conclude that asexual populations can gain most of the benefit of segregation through MR while avoiding the costs associated with sexual reproduction.


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