Worm Breeder's Gazette 12(4): 38 (October 1, 1992)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.


Diane Church, Eric Lambie

Department of Biology, Dartmouth College, Hanover, NH, 03755.

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 ( n1046 d)double mutants are Vul, but glv-1 ; lin-1 and glv-1 ; lin-12 ( n137 d)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.

Literature Cited:

Lambie and Kimble, abstract #186.