Peroxiredoxins (Prdx) are highly conserved, abundant antioxidant enzymes with multiple, diverse roles in responses to reactive oxygen species (ROS). ROS, such as hydrogen peroxide, are produced in cells during normal aerobic metabolism and in response to various stimuli and have the potential to cause oxidative damage. The peroxidase activity of peroxiredoxins has an important role in detoxifying hydrogen peroxide to prevent this damage. However, it is now widely accepted that hydrogen peroxide also has signaling functions and, in addition to their ROS-protective roles, peroxiredoxins are also important regulators of hydrogen peroxide signaling. Previous studies in C. elegans have shown that the thioredoxin peroxidase activity of the cytosolic 2-Cys Prdx, PRDX-2, is required in the intestine to protect against the toxic effects of exogenous hydrogen peroxide [1]. However, PRDX-2, is also required in other tissues for normal C. elegans growth and fecundity [1, 2]. Here, we investigated the basis for the reproductive defect of the
prdx-2 mutant. We have established that a shortened period of spermatogenesis contributes to the lower fecundity of
prdx-2 mutant and
prdx-2 RNAi-treated hermaphrodites. We find that
prdx-2 mutants exhibit a slight delay in larval development including the onset of hermaphrodite spermatogenesis. However, despite this developmental delay,
prdx-2 mutants switch prematurely from spermatogenesis to oogenesis resulting in the production of fewer sperm. Data will be presented from genetic studies to determine the underlying mechanism responsible for the premature switch to oogenesis in PRDX-2-deficient animals. There is a growing appreciation of the important role that ROS, such as hydrogen peroxide, play in regulating a variety of biological processes, including cell growth, differentiation and migration. Our data revealing that a peroxidase, PRDX-2, is required for the appropriate timing of the sperm/oocyte switch raises the intriguing possibility that ROS may also be intimately involved in controlling this cell fate decision. [1] Olahova M, Taylor SR, Khazaipoul S, Wang J, Morgan BA, Matsumoto K, Blackwell TK, Veal EA. (2008) PNAS 105(50):19839-19844. [2] Isermann K, Liebau E, Roeder T, Bruchhaus I. (2004) J Mol Biol. 338:745-55.