Transcriptional repressors of the polycomb group (PcG), together with the counteracting trithorax group (trxG) proteins, have been shown to regulate hox gene expression in flies and mammals. PcG proteins constitute two complexes, polycomb repressive complex 1 (PRC1) and the ESC-E(Z) complex. Sop-2 , a PcG like gene in C. elegans , encodes a protein with a SAM domain, a self-associating protein domain also found in PRC1 components polyhomeotic (PH) and sex combs on midleg (SCM). The function of
sop-2 is found to be analogous to that of PRC1. A
sop-2 loss of function mutation results in the ectopic expression of several hox genes. For example, in a
sop-2 mutant, C. elegans hox gene
egl-5 (Abd-B homolog) is expressed not only in several posterior tissues, but also ectopically in head neurons and anterior seam cells. SOP-2 is identified to be a RNA binding protein, having interaction with a zinc-finger RNA binding protein MEP-1 (Zhang et al., Mol. Cell , in press). Based on the above evidences, we hypothesize that
sop-2 might regulate
egl-5 expression post-transcriptionally via a regulatory element in the
egl-5 3 ' UTR. In order to asses whether regulation can occur via 3 ' UTR, we compared the expression patterns of two reporters using the V6 lineage cis -regulatory element (V6CRE), an enhancer of
egl-5 , to drive delta
pes-10 ::gfp expression with
unc-54 3 ' UTR and
elg-5 3 ' UTR, respectively. We found that whereas in the V6 lineage their expression is the same, the expression patterns of V6CRE-GFP-
unc-54 3 ' UTR and V6CRE-GFP-
egl-5 3 ' UTR are different in head neurons and gut cells. V6CRE-GFP-
unc-54 3 ' UTR is expressed in many head neurons and gut cells, while V6CRE-GFP-
egl-5 3 ' UTR is not. These differences indicate that regulation can occur through the 3 ' UTR. Moreover, in a
sop-2 mutant, V6CRE-GFP-
egl-5 3 ' UTR is expressed ectopically in anterior seam cells, and more head neurons than in wildtype, but far less than V6CRE-GFP-
unc-54 3 ' UTR. This result suggests that
sop-2 and other factors are recruited to regulatory elements on the
egl-5 3 ' UTR to regulate expression. In our effort to find the regulatory elements in the
egl-5 3 ' UTR, we identified a 5bp region required for repression in head neurons. This region has the same sequence as the point mutant element (PME) in
fem-3 3 ' UTR. The PME site is a binding site for FBF protein, which controls the switch from spermatogenesis to oogenesis in hermaphrodite worms by the repression of
fem-3 mRNA activity. With deletion of the PME site in the
egl-5 3 ' UTR, V6CRE-GFP-
egl-5 3 ' UTR is expressed in many more head neurons. However, it is likely that there are no specific sequences in the
egl-5 3 ' UTR responsible for repression in gut cells. Deletion of 1.5kb, 1.8kb and 2.5kb of downstream sequences in the
egl-5 3 ' UTR and even insertion of a 120bp sequence of the
egl-5 3 ' UTR before the
unc-54 3 ' UTR, had no observed effect on the expression pattern of gut cells. The binding sites for
sop-2 , other factors regulating expression as well as the regulation mechanism are still under investigation.