The
glp-1 gene encodes a transmembrane receptor that receives an inductive cue during embryonic and larval development. Zygotic
glp-1 expression is essential for induction of mitotic proliferation in the germline from L2 through adulthood. In the absence of
glp-1 function, cells that normally undergo mitosis enter meiosis. Maternal
glp-1 is needed for several inductive events during embryogenesis. Last year, we described an enhancer of
glp-1,
ego-1. This year, we report the latest molecular and genetic data with
ego-1, as well as with a more recently characterized gene,
ego-6. Both alleles of
ego-1,
om18 and
om71, have a reduced germline, abnormal oogenesis and never produce viable offspring. The defect in
om71 is slightly more pronounced.
ego-1 has been mapped to an interval between
lrp-1 and
gld-1 near the cluster of LGI. This area is spanned by a series of 4 overlapping cosmids. Southern blotting using these cosmids as probes did not reveal any RFLPs with either allele. Currently, mutagenesis is underway to generate more alleles. Also, the cosmids are being injected along with marker DNA in order to generate transgenic lines for testing for rescue of the
ego-1 phenotype. Genetic data indicate an unusual enhancement interaction between
ego-1 and another germline gene,
lag-1(
om13).
ego-1 alleles may act as dominant enhancers of the
lag-1(
om13ts) maternal effect lethality. Another gene,
ego-6 , is located just to the left of
ego-1. The phenotype of
ego-6 roughly parallels that of
ego-1 in terms of oogenesis defects and abnormal chromosomal morphology. We believe these to be separate genes since three factor map data are consistent; they place
ego-6 to the left of
ego-1. Also,
ego-1 fails to complement nDf25 while
ego-6 complements the same deficiency. Interestingly, the five alleles of
ego-6 exhibit intergenic noncomplementation with both alleles of
ego-1. These interactions are currently being analysed.