We have identified a potential binding site for Odd-skipped (ODD) proteins in the promoters of likely germline GLP-1 targets. MEME analysis identified a motif in the promoters of
sygl-1,
lst-1, and
fbf-2. JASPAR analysis indicated high similarity between the motif and binding sites for the Drosophila Odd and mouse Odd-skipped related 1 (OSR1) and 2 (OSR2) transcription factors. C. elegans has two odd homologs,
odd-1 and
odd-2. In 2004, Buckley, et al. showed that ODD-1/2 have non-redundant functions in the C. elegans intestine. Worms injected with
odd-1 or
odd-2 RNAi died as early larvae from intestinal defects. While intestinal ODD-1/2 expression was demonstrated with GFP, germline expression was not, possibly due to its presence on an array. Odd genes are involved in the development of many mammalian tissues and OSR1 has been implicated in gastric and pancreatic cancer. The Drosophila Odd proteins activate transcription, but have mostly been implicated in gene repression. We therefore hypothesized that odd genes might repress germline genes in non-germline C. elegans tissues. Preliminary results support this hypothesis. An in situ hybridization showed no hermaphrodite germline expression of
odd-2. We analyzed gene ontology of promoters containing the potential ODD binding site (OBS) compared to promoters without it. Analysis of affiliated anatomy terms using the statistical program R showed that genes with an OBS were slightly more likely (1.13x) to be associated with intestine (where the ODD protein is known to be expressed) than those without an OBS (P <.005). Germline terms, however, were 1.6x more likely to be associated with OBS-containing genes than those without (P < .00001). The
odd-2 gene is most closely related to the mammalian homologs and a larval lethal mutant of
odd-2 is available. We have initiated studies with an available
odd-2::GFP fusion (OP405) to determine germline expression by presence of GFP or in somatic-rescue phenotypes. The array is unstable, which may be a feature of
odd-2; Buckley, et al. could only maintain their strain for a few generations. When we have stable transgenes, we plan to perform biochemical studies to show whether ODD-1/ODD-2 bind this motif. We have also planned experiments to study expression of potential target genes in the embryos/early larvae of the
odd-2 mutant. For financial support, we would like to acknowledge the Kimble lab for the initial stages of this project, ECSU and the CSU-AAUP. .