We have previously reported the characterization of the
lin-12 hypomorphic allele
n676n930ts ,and our screen for reversion of the Egl defect of
n676n930ts hermaphrodites (WBG 10:2 p.83). Twenty seven EMS-induced extragenic suppressor mutations were obtained in this screen, at a total frequency of 5x10 +E-5.None has any obvious phenotype in a
lin-12 (+)background. Approximately half of the revertants contain dominant suppressors mapping near
dpy-5 on linkage group I; these appear to be equivalent to dominant suppressors of
glp-1 (
e2142)isolated by Jim Priess. Anne Marie Howell and Jim Priess have argued that these suppressors are loss of function mutations, and that dominant suppression is due to haplo-insufficiency (WBG 11:5 p. 92). Together with Howell and Priess, we have tentatively assigned these dominant suppressors to one locus which we are calling
slg-1 ,for suppressor of
lin-12 and
alp-1 . We have also identified recessive suppressors of the
lin-12 (
n676n930ts)Egl defect. Eleven of these define four complementation groups all mapping between
rol-3 and
unc-42 on linkage group V. We have named these the sel genes, for suppressor/enhancer of
lin-12 because suppressor mutations suppress hypomorphic
lin-12 alleles but enhance hypermorphic
lin-12 (d)alleles. Mutations in
sel-10 ,but not
sel-1 ,
sel-9 ,or
sel-11 ,are able to weakly suppress the
lin-12 (0)alleles
q269 and
n941 ,suggesting that
sel-10 may act downstream of
lin-12 . In order to determine the nature of the sel alleles, we have performed gene dosage studies using the duplications mnDp26 and ctDp11 ,and seven different deficiencies in the region, including mDf3 .In these experiments, we have scored suppression of the
lin-12 (
n676n930)Egl defect, as well as suppression of a specific cell fate transformation in the AC/VU decision. In general, we have found that sel/Df and sel/sel/+ suppress less well than sel/sel (or not at all). These experiments argue that all of the sel mutations are dosage sensitive gain of function alleles, and that sel(+) in some way antagonizes the activity of the suppressor allele.