Sibling rivalry versus mother's curse: can kin competition facilitate a response to selection on male mitochondria?
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ABSTRACT:
SUBMITTER: Keaney TA
PROVIDER: S-EPMC7423468 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Many essential organelles and endosymbionts exhibit a strict matrilineal pattern of inheritance. The absence of paternal transmission of such extranuclear components is thought to preclude a response to selection on their effects on male viability and fertility. We overturn this dogma by showing that two mechanisms, inbreeding and kin selection, allow mitochondria to respond to selection on both male viability and fertility. Even modest levels of inbreeding allow such a response to selection when there are direct fitness effects of mitochondria on male fertility because inbreeding associates male fertility traits with mitochondrial matrilines. Male viability effects of mitochondria are also selectable whenever there are indirect fitness effects of males on the fitness of their sisters. When either of these effects is sufficiently strong, we show that there are conditions that allow the spread of mitochondria with direct effects that are harmful to females, contrary to standard expectation. We discuss the implications of our findings for the evolution of organelles and endosymbionts and genomic conflict.
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Project description:UnlabelledMyxobacteria form complex social communities that elicit multicellular behaviors. One such behavior is kin recognition, in which cells identify siblings via their polymorphic TraA cell surface receptor, to transiently fuse outer membranes and exchange their contents. In addition, outer membrane exchange (OME) regulates behaviors, such as inhibition of wild-type Myxococcus xanthus (DK1622) from swarming. Here we monitored the fate of motile cells and surprisingly found they were killed by nonmotile siblings. The kill phenotype required OME (i.e., was TraA dependent). The genetic basis of killing was traced to ancestral strains used to construct DK1622. Specifically, the kill phenotype mapped to a large "polyploid prophage," Mx alpha. Sensitive strains contained a 200-kb deletion that removed two of three Mx alpha units. To explain these results, we suggest that Mx alpha expresses a toxin-antitoxin cassette that uses the OME machinery of M. xanthus to transfer a toxin that makes the population "addicted" to Mx alpha. Thus, siblings that lost Mx alpha units (no immunity) are killed by cells that harbor the element. To test this, an Mx alpha-harboring laboratory strain was engineered (by traA allele swap) to recognize a closely related species, Myxococcus fulvus. As a result, M. fulvus, which lacks Mx alpha, was killed. These TraA-mediated antagonisms provide an explanation for how kin recognition specificity might have evolved in myxobacteria. That is, recognition specificity is determined by polymorphisms in traA, which we hypothesize were selected for because OME with non-kin leads to lethal outcomes.ImportanceThe transition from single cell to multicellular life is considered a major evolutionary event. Myxobacteria have successfully made this transition. For example, in response to starvation, individual cells aggregate into multicellular fruiting bodies wherein cells differentiate into spores. To build fruits, cells need to recognize their siblings, and in part, this is mediated by the TraA cell surface receptor. Surprisingly, we report that TraA recognition can also involve sibling killing. We show that killing originates from a prophage-like element that has apparently hijacked the TraA system to deliver a toxin to kin. We hypothesize that this killing system has imposed selective pressures on kin recognition, which in turn has resulted in TraA polymorphisms and hence many different recognition groups.
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Project description:Mammal life history traits relating to growth and reproduction are extremely diverse. Sibling rivalry may contribute to selection pressures influencing this diversity, because individuals that are relatively large at birth typically have an advantage in competition for milk. However, selection for increased growth rate is likely to be constrained by kin selection and physiological costs. Here, we present and test a model examining the ESS (evolutionarily stable strategy) balance between these constraints and advantages associated with increased prenatal growth in mammal sibling rivalry. Predictions of the model are supported by results of comparative analyses for the Carnivora and Insectivora, which demonstrate an increase in prenatal growth rate with increasing intensity of postnatal scramble competition, and a decrease in postnatal growth rate relative to size at birth. Because increased prenatal growth rates are predicted to select for reduced gestation length under certain conditions, our study also indicates that sibling rivalry may contribute to selection pressures influencing variation in altriciality and precociality among mammals.
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Project description:Strict maternal inheritance renders the mitochondrial genome susceptible to accumulating mutations that harm males, but are otherwise benign or beneficial for females. This 'mother's curse' effect can degrade male survival and fertility if unopposed by counteracting evolutionary processes. Coadaptation between nuclear and mitochondrial genomes-with nuclear genes evolving to compensate for male-harming mitochondrial substitutions-may ultimately resolve mother's curse. However, males are still expected to incur a transient fitness cost during mito-nuclear coevolution, and it remains unclear how severe such costs should be. We present a population genetic analysis of mito-nuclear coadaptation to resolve mother's curse effects, and show that the magnitude of the 'male mitochondrial load'-the negative impact of mitochondrial substitutions on male fitness components-may be large, even when genetic variation for compensatory evolution is abundant. We also find that the male load is surprisingly sensitive to population size: male fitness costs of mito-nuclear coevolution are particularly pronounced in both small and large populations, and minimized in populations of intermediate size. Our results reveal complex interactions between demography and genetic constraints during the resolution of mother's curse, suggesting potentially widespread species differences in susceptibility to mother's curse effects.
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Project description:The maternal inheritance of mitochondrial genomes entails a sex-specific selective sieve, whereby mutations in mitochondrial DNA can only respond to selection acting on females. In theory, this enables male-harming mutations to accumulate in mitochondrial genomes as long as they are neutral, beneficial, or only slightly deleterious to females. Ultimately, this bias could drive the evolution of male-specific mitochondrial mutation loads, an idea known as mother's curse. Earlier work on this hypothesis has mainly used small Drosophila panels, in which naturally sourced mitochondrial genomes were coupled to an isogenic nuclear background. The lack of nuclear genetic variation in these designs has precluded robust generalization. Here, we test the predictions of mother's curse using a large Drosophila mitonuclear genetic panel, comprising nine isogenic nuclear genomes coupled to nine mitochondrial haplotypes, giving a total of 81 different mitonuclear genotypes. Following a predictive framework, we tested the mother's curse hypothesis by screening our panel for wing size. This trait is tightly correlated with overall body size and is sexually dimorphic in Drosophila. Moreover, growth is heavily reliant on metabolism and mitochondrial function, making wing size an ideal trait for the study of the impact of mitochondrial variation. We detect high levels of mitonuclear epistasis, and more importantly, we report that mitochondrial genetic variance is larger in male than female Drosophila for eight out of the nine nuclear genetic backgrounds used. These results demonstrate that the maternal inheritance of mitochondrial DNA does indeed modulate male life history traits in a more generalisable way than previously demonstrated.
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Project description:Traditional views of sexual selection assumed that male-male competition and female mate choice work in harmony, selecting upon the same traits in the same direction. However, we now know that this is not always the case and that these two mechanisms often impose conflicting selection on male sexual traits. Cuticular hydrocarbons (CHCs) have been shown to be linked to both social dominance and male attractiveness in several insect species. However, although several studies have estimated the strength and form of sexual selection imposed on male CHCs by female mate choice, none have established whether these chemical traits are also subject to sexual selection via male-male competition. Using a multivariate selection analysis, we estimate and compare sexual selection exerted by male-male competition and female mate choice on male CHC composition in the broad-horned flour beetle Gnatocerus cornutus. We show that male-male competition exerts strong linear selection on both overall CHC abundance and body size in males, while female mate choice exerts a mixture of linear and nonlinear selection, targeting not just the overall amount of CHCs expressed but the relative abundance of specific hydrocarbons as well. We discuss the potential implications of this antagonistic selection with regard to male reproductive success.
| S-EPMC4999037 | biostudies-literature
Project description:Many studies have assessed the costs of sibling rivalry in systems where offspring always have competitors, but conclusions about sibling rivalry in these species are restricted to interpreting the cost of changes in the relative level of competition and are often complicated by the expression of potentially costly rivalry related traits. Additionally, the majority of studies focus on early-life sibling rivalry, but the costs of competition can also affect later-life performance. We test a suite of hypothesized immediate (early-life body mass, telomere length, and survival) and delayed (adult reproductive potential and lifespan) costs of sibling rivalry for offspring of differing competitive ability in Seychelles warblers, where most offspring are raised singly and hence competitor success can be compared to a competition-free scenario. Compared to those raised alone, all competing nestlings had lower body mass and weaker competitors experienced reduced survival. However, the stronger competitors appeared to have longer adult breeding tenures and lifespan than those raised alone. We propose that comparisons with competition-free groups, as well as detailed fitness measures across entire lifetimes, are needed to understand the evolution of sibling rivalry and thus individual reproductive strategy in wild systems.
| S-EPMC5873840 | biostudies-literature
Project description:Sibling rivalry is commonplace within animal families, yet offspring can also work together to promote each other's fitness. Here we show that the extent of parental care can determine whether siblings evolve to compete or to cooperate. Our experiments focus on the burying beetle Nicrophorus vespilloides, which naturally provides variable levels of care to its larvae. We evolved replicate populations of burying beetles under two different regimes of parental care: Some populations were allowed to supply posthatching care to their young (Full Care), while others were not (No Care). After 22 generations of experimental evolution, we found that No Care larvae had evolved to be more cooperative, whereas Full Care larvae were more competitive. Greater levels of cooperation among larvae compensated for the fitness costs caused by parental absence, whereas parental care fully compensated for the fitness costs of sibling rivalry. We dissected the evolutionary mechanisms underlying these responses by measuring indirect genetic effects (IGEs) that occur when different sibling social environments induce the expression of more cooperative (or more competitive) behavior in focal larvae. We found that indirect genetic effects create a tipping point in the evolution of larval social behavior. Once the majority of offspring in a brood start to express cooperative (or competitive) behavior, they induce greater levels of cooperation (or competition) in their siblings. The resulting positive feedback loops rapidly lock larvae into evolving greater levels of cooperation in the absence of parental care and greater levels of rivalry when parents provide care.
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Project description:Bacteria can secrete a wide array of antibacterial compounds when competing with other bacteria for the same resources. Some of these compounds, such as bacteriocins, can affect bacteria of similar or closely related strains. In some cases, these secretions have been found to kill sibling cells that belong to the same colony. Here, we present experimental observations of competition between 2 sibling colonies of Paenibacillus dendritiformis grown on a low-nutrient agar gel. We find that neighboring colonies (growing from droplet inoculation) mutually inhibit growth through secretions that become lethal if the level exceeds a well-defined threshold. In contrast, within a single colony developing from a droplet inoculation, no growth inhibition is observed. However, growth inhibition and cell death are observed if material extracted from the agar between 2 growing colonies is introduced outside a growing single colony. To interpret the observations, we devised a simple mathematical model for the secretion of an antibacterial compound. Simulations of this model illustrate how secretions from neighboring colonies can be deadly, whereas secretions from a single colony growing from a droplet are not.
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Project description:UnlabelledNatural habitats vary in available nutrients and room for bacteria to grow, but successful colonization can lead to overcrowding and stress. Here we show that competing sibling colonies of Paenibacillus dendritiformis bacteria survive overcrowding by switching between two distinct vegetative phenotypes, motile rods and immotile cocci. Growing colonies of the rod-shaped bacteria produce a toxic protein, Slf, which kills cells of encroaching sibling colonies. However, sublethal concentrations of Slf induce some of the rods to switch to Slf-resistant cocci, which have distinct metabolic and resistance profiles, including resistance to cell wall antibiotics. Unlike dormant spores of P. dendritiformis, the cocci replicate. If cocci encounter conditions that favor rods, they secrete a signaling molecule that induces a switch to rods. Thus, in contrast to persister cells, P. dendritiformis bacteria adapt to changing environmental conditions by inducible and reversible phenotypic switching.ImportanceIn favorable environments, species may face space and nutrient limits due to overcrowding. Bacteria provide an excellent model for analyzing principles underlying overcrowding and regulation of density in nature, since their population dynamics can be easily and accurately assessed under controlled conditions. We describe a newly discovered mechanism for survival of a bacterial population during overcrowding. When competing with sibling colonies, Paenibacillus dendritiformis produces a lethal protein (Slf) that kills cells at the interface of encroaching colonies. Slf also induces a small proportion of the cells to switch from motile, rod-shaped cells to nonmotile, Slf-resistant, vegetative cocci. When crowding is reduced and nutrients are no longer limiting, the bacteria produce a signal that induces cocci to switch back to motile rods, allowing the population to spread. Genes encoding components of this phenotypic switching pathway are widespread among bacterial species, suggesting that this survival mechanism is not unique to P. dendritiformis.
| S-EPMC3104493 | biostudies-literature