Worm Breeder's Gazette 11(3): 58
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.
Most hermaphrodites homozygous for weak (viable) alleles of let-23 ( such as n1045 , sy1, or sy97) are Vulvaless. However, these alleles do not completely prevent a response to the inductive signal from the anchor cell. As previously reported (WBG10:3-133, 11:2-106), we have examined approximately 90,000 mutagenized F1 chromosome sets for suppressors of the Vul phenotype of these weak alleles in hopes of finding new genes involved in vulval induction, especially those controlling production of the inductive signal. We have recovered 42 independent alleles, at least 32 of which fall into a single large complementation group which we call sli-1 for suppressor of lineage defect. We have mapped a representative allele, sli-1(sy102), to the left of unc-2, which is on the far left arm of the X chromosome. We have not tested for allelism with any of Stuart Kim's suppressors of lin-10.Alleles of this complementation group show a complex pattern of complementation. For instance, sy102 and sy112 fail to complement sy114. However, sy102 complements sy112: 19/21 animals of the genotype let-23(sy1); + him-5(e1490)/dpy-11(e224) +; sli-1 (sy102)/sli- 1(sy112) are Egg-laying defective (Egl-), whereas 38% of let-23(sy1); sli-1(sy102) animals are Egl-, and less than 2% of let-23(sy1); sli-1( sy112) are Egl-. These results suggest that neither sy102 nor sy112 are nulls. Most of the alleles analyzed thus far are similar to sy102 in their interactions with other alleles. [See Figure 1] A substantial number of hermaphrodites of the genotype let-23(sy1); sli-1 are Multivulva for most of the alleles examined. However, all of the sli-1 alleles examined seem to have no phenotype in the absence of a homozygous let-23 mutation. Vulval induction (measured by cellular anatomy in Nomarski optics, where 100% is three VPCs induced to make vulval cells) reflects this: [See Figure 2] Suppression of the let-23(sy1) vulval defect is at least partially gonad dependent. In 3/3 let-23(sy1); sli-1(sy102) animals in which Z1- Z4 were ablated in the L1 and the ventral hypodermis was intact, no induction was observed. Additionally, in 6/6 animals in which Z1-Z4 were ablated and from 1-3 P cells were also damaged, 0/24 surviving VPCs were induced. In one other animal, in which there was other laser damage, P8.p divided to the four cell stage before the animal died. Two explanations are consistent with these data: either (1) sli- 1 is active in the gonad and is therefore gonad dependent or (2) sli-1 can only suppress the let-23(sy1) vulval defect in the presence of active let-23 gene product, and let-23 is only active in response to the inductive signal. Our results suggest that sli-1 interacts with let-23, potentially as a negative regulator.
