Several groups of muscles in C. elegans exhibit continuous rhythmic activity throughout the life span of the animal. This motor activity supports a constant search for food and its processing, which is vital for survival. This rhythmic behavior exemplifies an ultradian cycle also observed in other species. In humans, an ultradian clock controls heartbeat and breathing, among other processes. The most studied, but yet incompletelyunderstood rhythmic behavior in C. elegans is the defecation motor program. It consists of two sequential longitudinal contractions of the body, followed by expulsion of the gut content. It takes 50 seconds on average to repeat each cycle. It was shown that an inositol trisphosphate (IP3) receptor expressed in intestinal cells regulates the motor program, through triggering calcium oscillation (1). We report three proteins that function in intestinal cells and may contribute to the periodicity of posterior body wall muscle contraction (pBoc), the first step in the defecation cycle. F11E6.5 was identified as a predicted protein structurally similar to fatty acid (FA) elongases of the GNS1/SUR4 gene family. We showed that elimination of F11E6.5 activity significantly alters the FA composition of lipids in worms. These changes correlate with shorter (37.1 +/- 6.3 sec) pBoc intervals as compared to wild type N2. We hypothesized that F11E6.5 may contribute to pBoc cycle through regulation of IP3 production, dependent on FA composition of phosphoinositides (2). We also showed that F11E6.5 RNAi may compensate for
unc-43 and
dec-11 pBoc mutant phenotypes. In addition, we showed that a RNAi- mediated loss of F11E6.5 function is associated with a reduced body size and a pale intestine, suggestive of additional defects in nutrient storage. In contrast to the F11E6.5 RNAi phenotype, interference with voltage-gated potassium channel genes,
kqt-2 and
kqt-3 , led to long and irregular pBoc cycles (see also 3). This suggested that suppression of these potassium channels, compromised a signal transduction event either up- or downstream of the time-keeper. This may be through altering the membrane potential or structural properties of the membrane. We showed that
kqt-2 and
kqt-3 RNAi phenotypes are dominant in a
flr-1 ( lf ) background, resulting in worms that displayed long irregular pBoc intervals. Based on our observation that
kqt-2 and
kqt-3 RNAi phenotypes in L3 animals are wild type, we hypothesized that the mechanism controlling pBoc in C. elegans is flexible and stage-dependent. 1. Dal Santo et al, (1999). Cell, vol.98, 757-767. 2. Carricaburu and Fournier, (2001). Eur. J.Biochem. 268, 1238-1249. 3. Wei et al., (2001). Abstract. Thirteenth International C. elegans Meeting.