At the '91 worm meeting we reported the isolation of a sterile vulvaless mutation,
q425 (Lambie and Kimble, abstract #186). Since then, we have isolated an additional allele,
q484 ,and have designated the afflicted locus
glv-1 (for germline maturation and vulval induction defective; pronounced glove). Both alleles are recessive; homozygotes are sterile and vulvaless. The most notable aspect of the sterile phenotype is the inability of pre-oocyte nuclei to undergo maturation; hermaphrodites are able to produce sperm, but germline nuclei that are committed to oogenesis fail to exit pachynema and are not packaged into oocytes. Granular material similar to that usually found in oocytes accumulates in the oviduct. We suspect that the
glv-1 sterile phenotype results from a failure in intercellular signaling, but have yet to determine what combination of somatic cells and germ cells are involved in this signaling. The vulvaless defect of
glv-1 results from a complete lack of vulval induction. All VPCs adopt SH (tertiary) fates. Since the vulval induction signaling pathway is rapidly being filled in, we did epistasis experiments to see how
glv-1 fits into this picture. The bottom line is that
glv-1 appears to be acting somewhere between
let-60 ras and
lin-1 /lin-12 .
glv-1 (
q425);
let-60 (
n1046d)double mutants are Vul, but
glv-1 ;
lin-1 and
glv-1 ;
lin-12 (
n137d)double mutants are Muv. In addition,
glv-1 /+;
let-60 (
n1046)animals are usually nonMuv, i.e.
glv-1 is a semidominant suppressor of
let-60 (
n1046). We are pursuing the cloning of
glv-1 by refining its map position on the left arm of chromosome I and by microinjecting YACs that cover the area. We are also screening for additional mutants with similar sterile phenotypes in order to isolate additional alleles of
glv-1 as well as to identify other genes that act in meiotic maturation.