Worm Breeder's Gazette 9(1): 70b
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 are studying five extragenic mutations that suppress the Tra phenotype of her-1(n695) V (see preceding abstract): ct27 III (gamma- ray induced), n1091 III and ct49 III (allelic, EMS-induced; ct49 was isolated by Sean Burgess), and n1092 V and n1102 V (allelic, EMS- induced). ct27 III has a semi-dominant dpy phenotype in XX animals; XO animals are less severely Dpy and are abnormal males. Both ct27; n695 and ct27/+;n695 XX animals exhibit strong suppression of the n695 Tra phenotype. Because ct27 results in a phenotype somewhat similar to that caused by mutations in the chauvinist dpy genes (dpy's 21, 26, 27, 28) it may suppress n695 with an effect on X-chromosome expression. n1091 III has no apparent effect on XX or XO animals by itself, while ct49 III XX and XO animals are Dpy h we have not eliminated the possibility that this phenotype results from a second closely linked mutation). n1091;n695 XX animals are well suppressed; n1091/+;n695 XX animals are not. n1092 V and n1102 V map near unc-76 (about 5% from her-1). Neither appears to have any effect on XX or XO animals by itself. For n1092 and n1102, both n695 sup and n695 sup/n695 + XX animals show strong suppression. n695n1O91 XO, n695n1O92 XO, and n695n11O2 XO animals are all normal males (that is, they are apparently identical to n695 XO animals). This suggests that the EMS-induced suppressor mutations on III and V affect a process that is active in XX, but not XO, animals. For example, the genes identified by these mutations could be involved in turning off her-1 expression in XX animals.