Worm Breeder's Gazette 12(2): 103 (January 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.
We have previously reported the characterization of the lin-12 hypomorphic allele n676 n930ts ,and our screen for reversion of the Egl defect of n676 n930ts hermaphrodites (WBG 10:2 p.83). Twenty seven EMS-induced extragenic suppressor mutations were obtained in this screen, at a total frequency of 5 x10 +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 (n676 n930ts )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 ( n676 n930 )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.