When faced with an adverse environment, such as depletion of food, constitutively secreted C. elegans daumone (Jeong et al., 2005, Nature, 433, 451-455) signals this nematode to enter the dauer stage, an enduring and non-aged condition. We hypothesized that, like hibernating animals, C. elegans might also have the same molecular machine that controls energy consumption during the dauer stage. To understand the molecular mechanism by which dauer larvae manage energy metabolism, we were interested in cloning and characterizing C. elegans pyruvate dehydrogenase kinase (CePDK), which has been known to act as a molecular switch for hibernating animals by preventing the flow of glycolytic products into the tricarboxylic acid cycle under adverse conditions. Through an extensive homologue search and molecular cloning, we isolated the ZK370.5 clone, which was predicted to encode CePDK. Having established that the over-expressed recombinant CePDK in E. coli exhibited anticipated molecular characteristics, such as molecular size and catalytic function, the mRNA expression pattern was examined using quantitative RT-PCR. Our data showed that CePDK mRNA was highly expressed in both the dauer and starved states, but suppressed in other states, suggesting the presence of a regulatory mechanism by which the nutritional state can be sensitized by CePDK in C. elegans. When mRNA distribution was examined in several mutants that were grown under fed, starved and dauer conditions, the levels of CePDK gene expression were higher in both
daf-2 and
age-1 mutants than those in either
daf-16 or
nhr-49 mutants. In particular, RNAi of CePDK in
daf-2 mutants resulted in a reduced lifespan, indicating that PDK may also be regulated by DAF-16.