Sex and death

Cheng Shi, Coleen T. Murphy

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Sexual interactions negatively impact health and longevity in many species across the animal kingdom. C. elegans has been established as a good model to study how mating and intense sexual interactions influence longevity of the individuals. In this chapter, we review the most recent discoveries in this field. We first describe the phenotypes caused by intense mating, including shrinking, fat loss, and glycogen loss. We then describe three major mechanisms underlying mating-induced killing: germline activation, seminal fluid transfer, and male pheromone-mediated toxicity. Next, we summarize the current knowledge of genetic pathways involved in regulating mating-induced death, including DAF-9/DAF-12 steroid signaling, Insulin/IGF-1 signaling (IIS), and TOR signaling. Finally, we discuss the possible fitness benefits of mating-induced death. Throughout this review, we compare and contrast mating-induced death between the sexes and among different species in an effort to discuss this phenomenon and underlying mechanisms from the evolutionary perspective. Further investigation using mated C. elegans will improve our understanding of sexual antagonism, as well as the coordination between reproduction and somatic longevity in response to various external signals. Due to the evolutionary conservation in many aspects of mating-induced death, what we learn from a short-lived mated worm could provide new strategies to improve our own fitness and longevity.

Original languageEnglish (US)
Title of host publicationCurrent Topics in Developmental Biology
PublisherAcademic Press Inc.
DOIs
StateAccepted/In press - 2020

Publication series

NameCurrent Topics in Developmental Biology
ISSN (Print)0070-2153

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Cell Biology

Keywords

  • Germline
  • Insulin/IGF-1 signaling
  • Male pheromones
  • Mating-induced death
  • Seminal fluid
  • Sexual antagonism
  • Steroid signaling
  • TOR signaling

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