Biology subjects

Wild, G.

Publications and source records attributed to Wild, G..

5 recordsLinked to original sources

bioRxiv2024

Kin-discriminating partner choice promotes the evolution of helping

Kin selection theory predicts that individuals should evolve to help relatives, either by helping indiscriminately in a population where they do not move very far from their relatives, or by discriminating kin and conditionally helping them. It has been argued that, because kin discrimination enables individuals to reduce how helpful they are with some social partners as well increase how helpful they are with others, this could lead to an increase or a decrease in the overall level of helping, depending on the curvature of the function relating the optimal level of help and genetic relatedness. However, this prediction was based on a model in which individuals were not able to choose their social partners but only adjust how helpful they should be towards those social partners they have been allocated. Here, we perform a mathematical analysis showing that if kin discriminators are allowed to choose whom they help, kin discrimination is more likely to increase the overall level of helping than previously anticipated. We obtained these results in two complementary theoretical settings: one more general and the other more specific and concrete.

evolutionary biology↗

bioRxiv2023

Why Do Hybrids Turn Down Sex?

Asexual reproduction is ancestral in prokaryotes; the switch to sexuality in eukaryotes is one of the major transitions in the history of life. The study of the maintenance of sex in eukaryotes has raised considerable interest for decades and is still one of evolutionary biologys most prominent question. The observation that many asexual species are of hybrid origin have led some to propose that asexuality in hybrids results from sexual processes being disturbed because of incompatibilities between the two parental species genomes. This proximate theory appears difficult in real life, as it requires fundamental reproductive traits to be profoundly altered without collapsing individuals fertility. Repeated failures to produce asexual Amazon Molly in the lab through crossing experiments show that we are still in need of an evolutionary explanation. Here, we present a mathematical model and propose an adaptive route for the evolution of asexuality from previously sexual hybrids. Under smaller reproductive alterations, we show that asexuality can evolve to rescue hybrids reproduction. Importantly, we highlight that when incompatibilities only affect the fusion of sperm and eggs genomes, unreduced meiosis and paternal genome elimination can evolve separately, greatly facilitating the overall evolutionary route.

evolutionary biology↗

bioRxiv2022

The evolution of manipulative cheating

A social cheat is typically assumed to be an individual that does not perform a cooperative behaviour, or performs less of it, but can still exploit the cooperative behaviour of others. However, empirical data suggests that cheating can be more subtle, involving evolutionary arms races over the ability to both exploit and resist exploitation. These complications have not been captured by evolutionary theory, which lags behind empirical studies in this area. We bridge this gap with a mixture of game-theoretical models and individual-based simulations, examining what conditions favour more elaborate patterns of cheating. We found that as well as adjusting their own behaviour, individuals can be selected to manipulate the behaviour of others, which we term manipulative cheating. Further, we found that manipulative cheating can lead to dynamic oscillations (arms races), between selfishness, manipulation, and suppression of manipulation. Our results can help explain both variation in the level of cheating, and genetic variation in the extent to which individuals can be exploited by cheats.

evolutionary biology↗

bioRxiv2020

Epigenetic inheritance and the evolution of infectious diseases

Genes with identical DNA sequences may show differential expression because of epigenetic marks. These marks in pathogens are key to their virulence and are being evaluated as targets for medical treatment. Where epigenetic marks were created in response to past conditions (epigenetically inherited), they represent a form of memory, the impact of which has not been considered in the evolution of infectious diseases. We fill this gap by exploring the evolution of virulence in pathogens that inherit epigenetic information on the sex of their previous host. We show that memories of past hosts can also provide clues about the sex of present and future hosts when women and men differ in their immunity to infection and/or their interactions with the sexes. These biological and social differences between the sexes are pervasive in humans. We show that natural selection can favour the evolution of greater virulence in infections originating from one sex. Furthermore, natural selection can favour the evolution of greater virulence in infections across sexes (or within sexes). Our results explain certain patterns of virulence in diseases like measles, chickenpox and polio that have puzzled medical researchers for decades. In particular, they address why girls infected by boys (or boys infected by girls) are more likely to die from the infection than girls infected by girls (or boys infected by boys). We propose epigenetic therapies to treat infections by tampering with the memories of infecting pathogens. Counterintuitively, we predict that successful therapies should target pathogens genes that inhibit virulence, rather than those enhancing virulence. Our findings imply that pathogens can carry memories of past environments other than sex (e.g. those related to socioeconomic status) that may condition their virulence and could signify an important new direction in personalised medicine.

evolutionary biology↗

bioRxiv2019

Prophylactic host behaviour discourages pathogen exploitation

Much work has considered the evolution of pathogens, but little is known about how they respond to changes in host behaviour. We build a model where hosts are able to choose to engage in prophylactic measures that reduce the likelihood of disease transmission. This choice is mediated by costs and benefits associated with prophylaxis, but the fraction of hosts engaged in prophylaxis is also affected by population dynamics. We identify a critical cost threshold above which hosts do not engage in prophylaxis. Below the threshold, prophylactic host behaviour does occur and pathogen virulence, measured by the extent to which it exploits its host, is reduced by the action of selection relative to the level that would otherwise be predicted in the absence of prophylaxis. Our work emphasizes the significance of the dual nature of the trade-off faced by the pathogen between balancing transmission and recovery, and creating new infections in hosts engaging or not engaging in prophylaxis.

evolutionary biology↗