Biology subjects

Galipaud, M.

Publications and source records attributed to Galipaud, M..

3 recordsLinked to original sources

bioRxiv2022

Extrinsic mortality and senescence: a guide for the perplexed

Do environments or species traits that lower the mortality of individuals create selection for delaying senescence? Reading the literature creates an impression that mathematically oriented biologists cannot agree on the validity of George Williams prediction (who claimed yes). The abundance of models and opinions may bewilder those that are new to the field. Here we provide heuristics as well as simple models that outline when the Williams prediction holds, why there is a null model where extrinsic mortality does not change the evolution of senescence at all, and why it is also possible to expect the opposite of Williams prediction, where increased extrinsic mortality favours slower senescence. We hope to offer intuition by quantifying how much delaying the placement of an offspring into the population reduces its expected contribution to the gene pool of the future. Our first example shows why sometimes increased extrinsic mortality has no effect (the null result), and why density dependence can change that. Thereafter, a model with ten different choices for population regulation shows that high extrinsic mortality favours fast life histories (Williams) if increasing density harms the production of juveniles or their chances to recruit into the population. If instead increasing density harms the survival of older individuals in a population, then high extrinsic mortality favours slow life histories (anti-Williams). We discuss the possibility that empirically found Williams-like patterns provide indirect evidence for population regulation operating via harming the production or fitness prospects of juveniles, as opposed to the survival of established breeders.

evolutionary biology↗

bioRxiv2020

The Evolution of Immune Sensitivity under Immunopathological and Autoimmune Costs

Hosts with high immune sensitivity benefit from rapid recovery but suffer multiple costs thereof. We distinguish between immunopathological costs due to collateral damage and autoimmune costs due to false positives against self. Selection on sensitivity follows different trajectories depending on the cost nature and the overlap degree between host- and parasitic molecular signatures. Increased parasite virulence selects for higher immune sensitivity under immunopathological costs but low sensitivity when the costs are autoimmune, contradicting previous theoretical results. Longer lifespan of the host selects for low sensitivity under immunopathology to avoid accumulated tissue damage. Under autoimmune costs, hosts with a shorter lifespan cannot afford to shorten it further due to autoimmunity and evolve lower immune sensitivity. Longer lifespan selects for high or low sensitivity depending on the presence of immune memory. These results extend our understanding of selection on immune sensitivity and help explain phenomena like the cytokine shock and chronic infections.

evolutionary biology↗

bioRxiv2020

Transmissible cancers do not easily select for sexual reproduction

The predominance of sexual reproduction in eukaryotes remains paradoxical in evolutionary theory. Of the hypotheses proposed to resolve this paradox, the "Red Queen hypothesis" emphasizes the potential of antagonistic interactions to cause fluctuating selection, which favours the evolution and maintenance of sex. While empirical and theoretical developments have focused on host-parasite interactions, the premises of the Red Queen theory apply equally well to any type of antagonistic interactions. Recently, it has been suggested that early multicellular organisms with basic anticancer defenses were presumably plagued by antagonistic interactions with transmissible cancers, and that this could have played a pivotal role in the evolution of sex. Here, we dissect this argument using a population genetic model. One fundamental aspect distinguishing transmissible cancers from other parasites is the continual production of cancerous cell lines from hosts own tissues. We show that this influx dampens fluctuating selection and therefore makes the evolution of sex more difficult than in standard Red Queen models. Although coevolutionary cycling can remain sufficient to select for sex under some parameter regions of our model, we show that the size of those regions shrinks once we account for epidemiological constraints. Altogether, our results suggest that horizontal transmission of cancerous cells is unlikely to cause fluctuating selection favouring sexual reproduction. Nonetheless, we confirm that vertical transmission of cancerous cells can promote the evolution of sex through a separate mechanism, known as similarity selection, that does not depend on coevolutionary fluctuations.

evolutionary biology↗