In general, as the evolutionary theory "survival of the fittest" implies, the viability of an organism, such as human, is highly dependent on its ability to adapt to constant environmental and metabolic stresses such as drought and famine and its ability to reproduce. With the use of adult male Caenorhabditis elegans, we have observed that exposure to short-term starvation stress improves viability coupled with an enhanced oxidative and thermal stress response and improved reproductive fitness. To enable an organism to support life, and ensure its survival and subsequent recovery from stress, it is imaginable that molecular regulation of transcription and translation is tightly controlled. Previously, our laboratory have reported the increase in protein biosynthesis and ribosome biogenesis as well as their rapid turnover during the initial phase of starvation in C. elegans [1]. We hypothesize that this starvation-induced ribosome biogeny is part of the reprogramming during starvation to equip the ribosomes with particular ribosomal proteins (RP). To screen for the candidate RP gene, we did RNAi knockdown of several RP genes and observed their survival after starvation stress. Interestingly, we found a member of the large subunit RP gene,
rpl-11.2, and not its corresponding duplicated RP gene,
rpl-11.1, to be involved in the starvation-induced improvement in viability. Moreover, starvation-induced increase in global protein biosynthesis was also abolished in
rpl-11.2 knockdown worms. These preliminary data provide clues that RP genes, particularly RPL-11.2 is likely involved in mediating metabolic response during starvation stress.References:1. Tan, K.T., et al., Insulin/IGF-1 receptor signaling enhances biosynthetic activity and fat mobilization in the initial phase of starvation in adult male C. elegans. Cell Metab, 2011. 14(3): p. 390-402.