Biology subjects

Stephenson, J. F.

Publications and source records attributed to Stephenson, J. F..

6 recordsLinked to original sources

bioRxiv2025

Pace of life predicts parasite resistance and fecundity tolerance, but not mortality tolerance, among Trinidadian guppies, Poecilia reticulata

Host defence against parasites can include limiting parasite growth, resistance, limiting the mortality cost of infection, mortality tolerance, and limiting the reproductive cost of infection, fecundity tolerance. Theoretically, these three host strategies have very different epidemiological and evolutionary outcomes. In particular, because mortality tolerance increases parasite population size, it is under strong positive frequency-dependent selection and may therefore be less variable between populations than either resistance or fecundity tolerance. Additionally, host investment in each strategy can be expected to differ between populations that experience different ecological conditions. Here, we tested how populations of Trinidadian guppies Poecilia reticulata from the upper and lower courses of three rivers responded to experimental infection with a novel strain of Gyrodactylus turnbulli. In line with theoretical predictions, we found that lower course populations, previously shown to have faster paces of life, invested less in resistance and fecundity tolerance - but not mortality tolerance - than the upper course populations with slower paces of life. Our results indicate that this host-parasite interaction both conforms to evolutionary-epidemiological theoretical predictions, and is shaped by broader ecological conditions.

evolutionary biology↗

bioRxiv2025

Interplay between purging and admixture shapes genetic load in an invasive guppy population

Demographic history can shape the genetic load of populations by influencing the efficacy of selection, levels of heterozygosity, and the incorporation of new variants via gene flow. Understanding these dynamics is crucial for identifying threats to population viability and predicting evolutionary trajectories of invasive populations translocated by humans into non-native environments. We investigate these processes in Trinidadian guppies (Poecilia reticulata) by estimating genetic loads across multiple populations, with a particular focus on a single expanding population in which translocated individuals have rapidly spread and replaced native individuals. Overall, we observe the expected negative relationship between neutral genetic diversity and relative genetic load. In the translocated population, patterns differ between strongly and weakly deleterious mutations. Strongly deleterious alleles are purged at the isolated translocation site but tend to accumulate along the expansion front. In contrast, the genetic load estimated based on weakly deleterious variants declines along the expansion gradient. These differing patterns can be explained by admixture with native populations (which carried fewer weakly deleterious mutations) reducing the overall genetic load of the population at the expansion front. However, admixture has also increased genetic diversity and introduced new strongly deleterious alleles, thereby reversing the purging effect. Together, our findings illustrate the complex interactions determining genetic load in subdivided populations, offering important insights into the evolutionary aspects of biological invasions.

evolutionary biology↗

bioRxiv2024

Artificial Selection and the Skin Microbiome Independently Predict Parasite Resistance

Host responses to parasite infection involve several interacting systems. Host genetics determine much of the response, but it is increasingly clear that the host-associated microbiome also plays a role. Genetically determined systems and the microbiome can also interact; for example, the microbiome can modulate the immune response, and vice versa. However, it remains unclear how such interactions between the host immune system and the microbiome may influence the hosts overall response to parasites. To investigate how host genetics and the microbiome interact to shape responses to parasites, we imposed truncation selection on Trinidadian guppies (Poecilia reticulata) for low and high resistance to the specialist ectoparasite Gyrodactylus turnbulli. After 3-6 generations of breeding without parasites, we sampled the skin-associated microbiome and infected fish from each line. We applied Dirichlet Multinomial Modeling (DMM) machine-learning to identify bacterial community types across lines and evaluated how selection line and community type explained variations in infection severity. Our findings showed that among females, the resistant line had significantly lower infection severity, while the susceptible line had higher infection severity. Among males, only the susceptible line experienced higher infection severity compared to the other lines. Line did not explain skin microbial diversity, structure or composition. Our DMM analysis revealed three distinct bacterial community types, independent of artificial selection lines, which explained just as much variation in infection load as selection line. Overall, we found that the microbiome and host genetics independently predict infection severity, highlighting the microbiomes active role in host-parasite interactions.

ecology↗

bioRxiv2023

Infection affects guppy reproductive fitness and offspring parasite resistance

O_LIInfection imposes energetic costs on hosts. Hosts typically respond by shifting resources, potentially affecting the quantity and quality of offspring they produce. As the sexes differ in their optimal reproductive strategies, infection of mothers versus fathers may affect offspring quantity and quality in different ways. C_LIO_LIHere, we test how experimental infection of guppies Poecilia reticulata with the ectoparasite Gyrodactylus turnbulli affects parental reproductive fitness and offspring parasite resistance. We compared breeding pairs in which one or neither parent had previously been infected. C_LIO_LIIn terms of reproductive fitness, parental infection experience did not affect the size, body condition, or number of offspring produced, but fathers who experienced the heaviest infections produced offspring [~]55 days sooner than average. This result may represent terminal investment by the males most affected by infection, or may indicate that these males have a faster pace of life, investing in reproduction at the expense of parasite defence. C_LIO_LIWe found that offspring age, parental infection experience, and parental infection severity together strongly predicted offspring parasite resistance. Only among pairs in which one parent had been infected, older offspring, which were those born soonest after the parents infection, tended to experience heavier infections. This result may therefore reflect temporary infection-induced reductions in parental investment in offspring quality. Beyond this effect of offspring age, offspring of infected mothers experienced 105 fewer worm days than those of infected fathers: fathers, but not mothers, that experienced heavy infections themselves produced offspring that also experienced heavy infections. The parent-offspring regression for infected fathers is therefore consistent with previous evidence that parasite resistance is heritable in this system, and yields a narrow sense heritability estimate of 0.69{+/-}0.13. By contrast, the mother-offspring regression (slope: -0.13{+/-}0.17) provides novel insight that mothers may engage in transgenerational immune priming. C_LIO_LIOverall, our results suggest that the sexes strike a different balance between offspring quantity and quality when faced with infection, with potentially broad implications for disease and host-parasite coevolutionary dynamics in nature. C_LI

ecology↗

bioRxiv2023

Associating with kin selects against disease tolerance

Behavioural and physiological immunity are key to slowing epidemic spread. Here, we explore the evolutionary and epidemic consequences of their different costs for the evolution of tolerance vs. resistance: behavioural resistance affects social cohesion, with associated group-level costs, while physiological resistance costs should accrue to the individual. Further, the transmission-reduction benefits of resistance accrue differently to susceptible hosts and those already infected; infected hosts only benefit indirectly, by reducing transmission to kin. We therefore model the coevolution of transmission-reducing defences expressed in susceptible hosts with those expressed in infected hosts, as a function of kin association, and analyse the effect on population-level outcomes. Using parameter values for guppies, Poecilia reticulata, and their gyrodactylid parasites, we find that: 1) either susceptible or infected hosts should invest heavily in preventing infection, but not both; 2) kin association drives investment in physiological resistance more strongly than in behavioural resistance; 3) even weak levels of kin association can favour altruistic infected hosts that invest heavily in resistance (vs. selfish tolerance), eliminating the disease. Overall, our finding that weak kin association affects the coevolution of infected and susceptible investment in both behavioural and physiological immunity suggests that kin selection may affect disease dynamics across systems.

evolutionary biology↗

bioRxiv2021

Social hosts evade predation but have deadlier parasites

Parasites exploit hosts to replicate and transmit, but overexploitation kills host and parasite (1): predators may shift this cost-benefit balance by consuming hosts (2-4) or changing host behavior, but the strength of these effects remains unclear. Modeling both, we find a primary, strong effect: hosts group to defend against predators (5), increasing parasite transmission, thus multiple infections, and therefore favoring more exploitative, virulent, parasites (6). Indeed, among 18 Trinidadian Gyrodactyus spp. parasite lines, those collected from high predation guppy populations were more virulent in common garden than those from low predation populations. Our model accurately predicted this result when parametrized with our experimentally demonstrated virulence-transmission trade-off, implicating the behavioral effects of predation. Broadly, our results indicate that reduced social contact selects against parasite virulence. One-Sentence SummaryOur theory and data show predators cause increased host social grouping; the resulting transmission favors parasite virulence.

ecology↗