Sex as a response to oxidative stress: A two-fold increase in cellular reactive oxygen species activates sex genes

Aurora M. Nedelcu^1*, Oana Marcu², and Richard E. Michod³

¹Department of Biology, University of New Brunswick, Fredericton, New Brunswick, Canada E3B 6E1

²Department of Developmental and Cell Biology, University of California, Irvine, California, 92697, USA

³Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, Arizona, 85721, USA

*Author for correspondence (anedelcu@unb.ca)

Key words: oxidative stress; reactive oxygen species; facultatively sexual species; sexual induction; Volvox carteri

Abstract

Organisms are constantly subjected to factors that can alter the cellular redox balance and result in the formation of a series of highly reactive molecules known as reactive oxygen species (ROS). As ROS can be damaging to biological structures, cells evolved a series of mechanisms (e.g., cell-cycle arrest, programmed cell death) to respond to high levels of ROS (i.e., oxidative stress). Recently, we presented evidence that in a facultatively sexual lineage – the multicellular green alga Volvox carteri – sex is an additional response to increased levels of stress, and likely ROS and DNA damage. Here, we show that in V. carteri (i) sex is triggered by a ca. two-fold increase in the level of cellular ROS (induced either by the natural sex-inducing stress, namely heat, or by blocking the mitochondrial electron transport chain with antimycin A), and (ii) ROS are responsible for the activation of sex genes. As most types of stress result in the overproduction of ROS, we believe that our findings will prove to extend to other facultatively sexual lineages, which could be indicative of the ancestral role of sex as an adaptive response to stress and ROS-induced DNA damage.