Normal hermaphrodite germline development requires coordination of molecules controlling proliferation, entry into meiosis, progression through meiotic prophase, and differentiation of sperm and oocytes. We have devised a mutational scheme to identify molecules involved in two of these processes, the control of germ cell proliferation and entry into the meiotic pathway. We reasoned that a reduction in products normally involved in either promoting entry into meiosis or inhibiting proliferation should result in excess proliferation. However, this phenotype may not be observed in a wild-type background, since proliferation in the distal germline requires a localized source of ligand [1,2,3]. To circumvent this problem, we conducted the mutational analysis in a
glp-1(
oz112oz120) genetic background where ligand-independent excess proliferation is observed in 0.05% of gonad arms [4]. From 9000 haploid genomes, we isolated 12 enhancers, designated as teg (tumorous enhancers of
glp-1(
oz112oz120)) alleles, that cause a
glp-1(
oz112oz120) dependent tumorous phenotype. In a
glp-1(+) background, none of the Teg mutants display an obvious germline phenotype. The teg loci have been mapped to individual chromosomes on the basis of their enhancer phenotypes with detailed three-factor mapping continuing. In addition, our screen may yield loss-of-function mutations in negative regulators of the GLP-1 signalling pathway [5, 6, 7]. Potential negative regulators have been identified in previous screens for suppressors and enhancers of
glp-1 (sog, suppressor of
glp-1) and
lin-12 (sel, suppressor and enhancer of
lin-12) [5, 6, 7]. To determine if any of the sog or sel genes enhance the tumorous germline phenotype of
glp-1(
oz112oz120), we are currently constructing strains mutant for
glp-1(
oz112oz120) and selected sog or sel mutations. Several of the sog genes, specifically
sog-1, 3, 5, and 10 are capable of enhancing the tumorous phenotype of
glp-1(
oz112oz120). However, at least three of the Teg mutants appear to identify genes distinct from known sog or sel genes. The possibility that these teg genes can suppress
glp-1(lf) phenotypes or enhance
lin-12(gf) mutants is being investigated. [1] Crittenden et al., 1994; [2] Tax et al., 1994; [3] Henderson et al., 1994; [4] Berry et al., 1997; [5] Maine and Kimble, 1993; [6] Sundaram and Greenwald, 1993; [7] Tax et al., in preparation. This work was supported by NIH Grant HD25614.