Effects of sex, mating status, and genetic background on circadian behavior in Drosophila

Front Neurosci. 2025 Jan 8:18:1532868. doi: 10.3389/fnins.2024.1532868. eCollection 2024.

Abstract

Circadian rhythms play a crucial role in regulating behavior, physiology, and health. Sexual dimorphism, a widespread phenomenon across species, influences circadian behaviors. Additionally, post-mating physiological changes in females are known to modulate various behaviors, yet their effects on circadian rhythms remain underexplored. Here, using Drosophila melanogaster, a powerful model for studying circadian mechanisms, we systematically assessed the impact of sex and mating status on circadian behavior. We measured circadian period length and rhythm strength in virgin and mated males and females, including females mated to males lacking Sex Peptide (SP), a key mediator of post-mating changes. Across four wild-type and control strains, we found that males consistently exhibited shorter circadian periods than females, regardless of mating status, suggesting that circadian period length is a robust sexually dimorphic trait. In contrast, rhythm strength was influenced by the interaction between sex and mating status, with female mating generally reducing rhythm strength in the presence of SP signaling. Notably, genetic background significantly modulated these effects on rhythm strength. Our findings demonstrate that while circadian period length is a stable sex-specific trait, rhythm strength is shaped by a complex interplay between sex, mating status, and genetic background. This study advances our understanding of how sex and mating influence circadian rhythms in Drosophila and provides a foundation for future research into sexually dimorphic mechanisms underlying human diseases associated with circadian disruptions.

Keywords: Drosophila; circadian behavior; circadian period; genetic background; mating effect; rhythm strength; sex peptide; sexual dimorphism.

Grants and funding

The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from the National Institutes of Health (R01NS086887 and R01NS109151 to KK) and funds from the Thomas Jefferson University Synaptic Biology Center (to KK).