Here you will find information on the evolution of sex and the role of oxidative stress in the evolution of sex in the Volvocales. Enjoy!

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Adaptive Value of Sex in Microbial Pathogens

Explaining the adaptive value of sex is one of the great outstanding problems in biology. The challenge comes from the difficulty in identifying the benefits provided by sex, which must outweigh the substantial costs of sex. Here, we consider the adaptive value of sex in viruses, bacteria and fungi, and particularly the information available on the adaptive role of sex in pathogenic microorganisms. Our general theme is that the varied aspects of sex in pathogens illustrate the varied issues surrounding the evolution of sex generally. These include, the benefits of sex (in the short and long term), as well as the costs of sex (both to the host and to the pathogen). For the benefits of sex (that is, its adaptive value), we consider three hypotheses: (i) sex provides for effective and efficient recombinational repair of DNA damages, (ii) sex provides DNA for food, and (iii) sex produces variation and reduces genetic associations among alleles under selection. Although the evolution of sex in microbial pathogens illustrates these general issues, our paper is not a general review of theories for the evolution of sex in all organisms. Rather, we focus on the adaptive value of sex in microbial pathogens and conclude that in terms of short-term benefits, the DNA repair hypothesis has the most support and is the most generally applicable hypothesis in this group. In particular, recombinational repair of DNA damages may substantially benefit pathogens when challenged by the oxidative defenses of the host. However, in the long term, sex may help get rid of mutations, increase the rate of adaptation of the population, and, in pathogens, may infrequently create new infective strains. An additional general issue about sex illustrated by pathogens is that some of the most interesting consequences of sex are not necessarily the reasons for which sex evolved. For example, antibiotic resistance may be transferred by bacterial sex, but this transfer is probably not the reason sex evolved in bacteria. Published in Infection, Genetics and Evolution (PDF)

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

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. Nedelcu A.M., Marcu O. and Michod R.E. (2004). Sex as a response to oxidative stress: A two-fold increase in cellular reactive oxygen species activates sex genes. Proc. Roy. Soc. B. In Press. (306KB PDF)

Sex as a response to oxidative stress: the effect of antioxidants on sexual induction in a facultatively sexual lineage

The evolution of sex is one of the long-standing unsolved problems in biology. Although in many lineages sex is an obligatory part of the life cycle and is associated with reproduction, in prokaryotes and many lower eukaryotes, sex is facultative, occurs in response to stress and often involves the formation of a stress-resistant dormant form. The proximate and ultimate causes of the connection between stress and sex in facultatively sexual lineages are unclear. Because most forms of stress result in the overproduction of cellular reactive oxygen species (ROS), we address the hypothesis that this connection involves ROS and possibly reflects the ancestral role of sex as an adaptive response to the damaging effects of stress-induced ROS (i.e. oxidative stress). Here, we report that two antioxidants inhibit sexual induction in a facultatively sexual species—the multicellular green alga, Volvox carteri. Furthermore, the nature of the sex response and the effect of an iron chelator on sexual induction are consistent with sex being a response to the DNA-damaging effects of ROS. In addition, we present preliminary data to suggest that sex, cell-cycle arrest and apoptosis are alternative responses to increased levels of oxidative stress. Nedelcu A.M., Michod R.E. (2003). Sex as a response to oxidative stress: The effect of antioxidants on sexual induction in a facultatively sexual lineage. Proc. R. Soc. Lond. B (Suppl. ) 270, S136-S139. (282KB PDF)

Heat Stress and Sex in V. carteri

See Figure 1 for the development of a sexual juvenile with eggs.

Sex as a response to oxidative stress: stress genes co-opted for sex

Additional support for the importance of stress in the evolution of sex can be found in a recent paper by A. Nedelcu. In the papers above, we showed that in the multicellular green alga, Volvox carteri, sex is a response to increased levels of reactive oxygen species (ROS), which could be indicative of the ancestral role of sex as an adaptive response to stress-induced ROS. To provide additional support for the suggestion that sex evolved as a response to oxidative stress, Nedelcu's study addresses the hypothesis that genes involved in sexual induction are evolutionarily related to genes associated with various stress responses. In particular, her study investigates the evolutionary history of genes specific to the sexual induction process in V. carteri—including those encoding the sexual inducer (SI) and several SI-induced extracellular matrix (ECM) proteins. Surprisingly, (i) a highly diversified multigene family with similarity to the V. carteri SI and SI-induced pherophorin family is present in its unicellular relative, Chlamydomonas reinhardtii (which lacks both a SI and an ECM) and (ii) at least half of the 12 identified gene members are induced (as inferred from reported expressed sequence tags) under various stress conditions. These findings suggest an evolutionary connection between sex and stress at the gene level, via duplication and/or co-option. Nedelcu, A.M. 2005 Proc. R. Soc. Lond. B 272, 1471-2954. (PDF)