Worm Breeder's Gazette 13(3): 61 (June 1, 1994)

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.

A polyray-1 suppressor

Julin Maloof, Cynthia Kenyon

Dept of Biochemistry, U.C.S.F, San Francisco, CA 94143

The polyray-1 ( pry-1 )gene is required to keep homeotic selector (HOM-C) genes repressed where their expression has not been initiated (see accompanying abstract and WBG 12(5):39). pry-1 mutant worms have numerous homeotic transformations and are very sick, so we were intrigued by a plate of pry-1 mutant worms which appeared much healthier than normal. I outcrossed the strain and found F2 swith the full pry-1 mutant phenotype, suggesting that the "healthy" strain contained both pry-1 and an extragenic suppressor. Does the suppressor have a phenotype on its own? Since pry-1 causes homeotic transformations due to ectopic HOM-C expression, it seemed possible that the suppressor would cause transformations in the opposite direction, similar to those seen in HOM-C loss of function mutants. Indeed some F2 sfrom the outcross had descendants of the QL neuroblast in the anterior of the worms, a phenotype also caused by loss-of-function mutations in the HOM-C gene mab-5 .We are calling this newly identified gene spy-1 for suppressor of polyray-1. spy-1 seems to suppress all of the pry-1 mutant phenotypes: pry-1 ; spy-1 double mutant worms do not have extra rays, are no longer Muv, are not Unc, and have anteriorly placed QR descendants. spy-1 could suppress pry-1 either by preventing ectopic HOM-C expression, or by preventing ectopically expressed HOM-C genes from having any effect. mab-5 -lacZexpression was examined and found to be normal in the pry-1 ; spy-1 double, so wild-type spy-1 is required for the ectopic HOM-C expression seen in pry-1 mutant animals. The fact that there is a QL migration defect in worms mutant for spy-1 alone suggests that spy-1 may normally be required to turn on mab-5 in QL. We compared expression of mab-5 -lacZin wild-type and spy-1 mutant worms at 3.5-5 hours and at 8-10 hours after hatching. At 3.5-5 hours 100% (n=20) of the mutant and 95% (n=20) of the wild-type worms had expression in QL. At 8-10 hours 0% (n=30) of the mutant worms has expression of mab-5 in the descendants of QL, but 87% (n=30) of the wild-type worms showed expression. It appears that spy-1 is not required to initiate mab-5 expression in QL, but that it is required to maintain expression once it is initiated. It is possible that spy-1 is required to maintain the ON state of a number of HOM-C genes, in a manner analogous to the brahma and trithorax genes of Drosophila. spy-1 is located on X, in a region well covered by cosmids. Hopefully a molecular analysis of spy-1 along with the isolation and study of more spy-1 alleles will enable us to determine how similar the C. elegans and Drosophila maintenance systems are, and how spy-1 and other maintenance genes are used to maintain and specify pattern.