To form the proximal-distal axis of the C. elegans gonad, two somatic gonadal precursor cells, Z1 and Z4, divide asymmetrically to generate one daughter with a proximal fate and one with a distal fate. Genes governing this process include the
lin-17 frizzled receptor,
wrm-1/beta-catenin, the
pop-1/TCF transcription factor,
lit-1/nemo-like kinase, and the
sys-1 gene. Normally, all of these regulators promote the distal fate. Here we show that nuclear levels of a
pop-1 GFP fusion protein are less abundant in the distal than in the proximal Z1/Z4 daughters. This POP-1 asymmetry is lost in mutants disrupting Wnt/MAPK regulation, but retained in
sys-1 mutants. We find that
sys-1 is haplo-insufficient for gonadogenesis defects and that
sys-1 and
pop-1 mutants display a strong genetic interaction in double heterozygotes. Therefore,
sys-1 is a dose-sensitive locus and may function together with
pop-1 to control Z1/Z4 asymmetry. To identify other regulatory genes in this process, we screened for mutants resembling
sys-1. Four such genes were identified (
gon-14, -15, -16 and
sys-3) and shown to interact genetically with
sys-1. However, only
sys-3 promotes the distal fate at the expense of the proximal fate. We suggest that
sys-3 is a new key gene in this pathway and that
gon-14,
gon-15 and
gon-16 may cooperate with POP-1 and SYS-1 at multiple stages of gonad