Worm Breeder's Gazette 13(5): 23 (February 1, 1995)
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.
Department of Biological Sciences, Dartmouth College, Hanover, NH 03755.
We are in the process of trying to determine how exit from pachytene
is regulated during gametogenesis. So far, we have found that exit from
pachytene is prevented by mutations in three components of the vulval
induction pathway: let-60(ras), mek-2(MAP kinase kinase; a.k.a. let-537
a.k.a. glv-1) and mpk-1(MAP kinase; a.k.a. sur-1). At present, we do not
know the identity of the genes that act upstream of let-60(ras) to
initiate signaling or from which tissue(s) the signal(s) originates .
Neither lin-1 nor lin-12, which operate downstream of mpk-1 during vulval
induction, appears to be important in regulating exit from pachytene. We
have recently identified a single allele of a gene that may act downstream
of mpk-1 in the germline. dx8 is recessive and causes essentially the
same germline phenotype as mutations in mpk-1 and mek-2. However, vulval
induction is not affected by dx8. The Muv phenotype caused by the
constitutively activated let-60 allele, n1046, is unaffected by dx8.
Moreover, the sterile phenotype of dx8 is not suppressed by n1046, leading
us to believe that dx8 may define a gene that functions downstream of
let-60 (and possibly downstream of mpk-1). dx8 maps just to the left of
unc-101, within a sparsely populated region of IR. As a prelude to
cloning, we are positioning dx8 more precisely via polymorphism mapping.
We are also attempting to generate more alleles in order to determine
whether the phenotype caused by dx8 is representative of a loss of gene
activity.