The DM domain transcription factor
mab-3 , like its Drosophila homologue doublesex (dsx) , regulates diverse male-specific traits that include expression of yolk in the intestine and the development of male-specific nervous system structures. In the C. elegans male tail,
mab-3 is required for differentiation of V rays, male sensory structures that are required for mating. In
mab-3 mutant males, the V5- and V6-derived neuroblasts fail to generate the sensory neurons and support cells that comprise the adult V rays, and instead differentiate primarily as hypodermal cells. While it has been clearly demonstrated that MAB-3 acts directly to repress yolk transcription in the male intestine 1 , less is understood about the role of
mab-3 in V ray differentiation. We have recently shown that
mab-3 is not absolutely required for V ray formation; overexpression of the bHLH gene
lin-32 can direct V ray differentiation in the absence of
mab-3 . We propose that
lin-32 acts as a primary determinant of V ray fate, while
mab-3 acts to potentiate
lin-32 activity 2 . Thus
mab-3 and
lin-32 act in concert to promote differentiation of the V5- and V6-derived neuroblasts. To better understand the mechanisms by which the
mab-3 and
lin-32 pathways converge to direct V ray development, we are currently screening for mutations that suppress the
mab-3(
e1240) lack of V rays. We expect this screen to reveal targets of
mab-3 regulation as well as genes that compensate for loss of
mab-3 by upregulating activity of the
lin-32 pathway. We have identified two mutations,
ez1 and
ez2 , which confer a phenotype that we have provisionally called Smt ( S uppressor of m ab in t ail). Both
ez1 and
ez2 act recessively to suppress
mab-3(
e1240) , partially restoring V ray formation. Suppression by
ez1 and
ez2 is sensory ray-specific; neither mutation suppresses the ectopic yolk expression in the
mab-3(
e1240) male intestine. Progress toward characterizing
ez1 and
ez2 and isolating additional suppressors will be reported. Identifying the nature of mutations that suppress
mab-3 will provide insight into the genes that act with
mab-3 and
lin-32 to direct male peripheral nervous system development. Finding homologues of these
mab-3 suppressors may reveal whether conservation between
mab-3 and dsx extends to include additional downstream regulators of male sexual development. 1 Yi and Zarkower (1999). Development 126: 873-877. 2 Yi et al. (2000). Development 127: 4469-4480.