The process of organogenesis involves cell proliferation, differentiation and morphogenesis. We have chosen the gonad as a model system to study the coordination of these events. The somatic structures of the gonad develop from two cells (Z1 and Z4) in the gonad primordium. In the wild type, Z1 and Z4 give rise to non-equivalent sister cells during L1. In hermaphrodites, Z1.a and Z4.p give rise to a distal tip cell (DTC), while Z1.p and Z4.a give rise to an AC/VU precursor. In males, Z1.a and Z4.p give rise to DTCs, while Z1.p and Z4.a give rise to the linker cell (LC). In addition to these regulatory cells, somatic blast cells are also generated, which become rearranged into a somatic primordium (SP) that prefigures the development of later somatic structures. We have isolated a collection of mutants that are defective in early gonadogenesis and are therefore sterile. Our recent focus has been on one group of these mutants that have similar early gonadal defects in hermaphrodites: loss of DTCs and the inability to form an SP. By mapping and complementation tests, we find that these mutations define six genes, designated
sys-1 through
sys-6 ( sys for sy mmetrical s isters ). Previous work demonstrated that the first divisions of Z1 and Z4 appear to generate equivalent cells in
sys-1 hermaphrodites -- Z1.a and Z4.p appear to adopt the fates of their sisters(1). This phenotype is similar to that described for the frizzled homologue
lin-17 (2) . Furthermore, the two
sys-2 mutations are actually alleles of
pop-1, consistent with the idea that the Wnt signaling pathway controls the polarity of this first division (see Siegfried abstract). Here we report our progress on characterizing
sys-3 -
sys-6. The
sys-2 -
sys-6 genes and
lin-17 not only have similar phenotypes, but they also interact genetically with
sys-1. Thus, for example,
sys-1/ +;
sys-4/ + double heterozygotes display Sys gonadal phenotypes even though both mutations are normally recessive. These genetic interactions suggest that the sys genes and
lin-17 all function in a common pathway to control early gonadal development. However, with the exception of
sys-2 , the other sys genes do not map to any known Wnt pathway components. Therefore, the sys genes may identify regulators of Wnt signaling that have previously not been identified. 1. Miskowski et al. (2001) Developmental Biology 230, 61-73. 2. Sternberg and Horvitz (1988) Developmental Biology 130, 67-73.