“good genes” sexual selection stipulates that a positive additive genetic correlation exists between sexual success and non-sexual success. Despite the solid theoretical framework, findings from empirical research remain ambiguous. This thesis explores the “good genes” hypothesis and investigates the role of pathogens in sexual selection with an emphasis on including various epidemiological contexts for sexual selection and the realization of the potential “good genes”, using a trio system of Drosophila melanogaster, the fungus Metarhizium brunneum, and the gram-negative bacterium Pseudomonas entomophila.
Chapter 1 looks into the impacts of fungal infection on male reproductive potential in non-competing settings to evaluate the potential role of sexual selection in promoting resistant genes. Despite the strongly aroused immune responses and high mortality, little impact was revealed. Chapter 2 shifts focus to investigate how much offspring fitness can be gained through female pathogen avoidance. Females actively avoided infectious oviposition sites, but no fitness penalty was found for laying eggs on fungi-contaminated sites.
Subsequent chapters explore whether and how pathogens mediate sexual selection in promoting offspring fitness. Chapter 3 asks how the presence of M.brunneum in the sexual selection context affects the link between sire sexual success (sire paternity share) and offspring pathogen resistance (survival post infection), showing that the sign of the correlation was mediated by the pathogen occurrence and was sex-specific. Infected sires had reduced sexual success, yet those of higher resistance achieved greater sexual success when competing for mates, suggesting a potential for sexual selection in promoting pathogen resistance. However, no positive link was found between sire sexual success and offspring pathogen resistance, challenging the “good genes” hypothesis. Chapter 4 broadens the scope by introducing P.entomophila to the offspring generation and assessing the offspring reproductive fitness (relative contribution to the grand-offspring generation) across various epidemiological contexts. Weak evidence was found showing the sex-specific/biased selection on offspring fitness-related traits. Although no correlation was found between sire sexual success and offspring reproductive fitness within any specific pathogenic context, weak evidence suggests a difference in the observed sire-offspring relationship depending on whether the environment of the sire and the offspring align or not.
In summary, findings from this thesis challenge the “good genes” hypothesis and underscore the necessity of including various contexts (e.g., occurrence of pathogens, offspring sex) in experimental design.