Worm Breeder's Gazette 12(4): 66 (October 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.
(1) Complex epistasis
We have been studying fluoride-resistant mutants of C. elegans (Katsura, Kondo and Amano: the 1991 C. elegans Meeting Abstract p179 ).The mutants can be classified into two classes. Class 1 mutants are resistant to 400 mg/ml NaF and grow slowly even in the absence of NaF. Class 2 mutants are not completely resistant to 400 mg/ml NaF and grow normally in the absence of NaF. Class 1-class 2 double mutants are resistant to 400 mg/ml and grow normally in the absence and presence of NaF. Namely, class 1 mutations are epistatic to class 2 mutations concerning degree of fluoride-resistance but hypostatic concerning growth rate. We have reported flr-1 Xand flr-3 IVas class 1 genes and flr-2 Vas a class 2 gene. Here we report flr-4 Xas a new class 1 gene and flr-5 (LG not yet determined) and flr-6 Vas new class 2 genes. The latter two mutations were obtained as suppressors of the slow-growing phenotype of class 1 mutants. We have cloned a 3.6kb EcoRI fragment containing Tc1 that caused flr-3 ( ut9 ),a spontaneous mutation isolated from a mut-5 strain.
(2) Clr-1 phenotype lethals
In the course of studying larval lethal mutations that affect gross morphology of worms we found that quite a few mutants have a phenotype similar to clr-1 mutants, that is, the intestine and the body wall are gradually detached during larval growth. We reported that one of them mapped in clr-1 ,and another in let-23 (Katsura, Kondo and Kawase: WBG 12(2) p108 ).After that we mapped one of them ( ut58 )in let-341 .Two of them ( ut103 and ut105 )were sent to Dr. J. Kimble's Lab and shown to be deletions that remove lag-2 gene (E. Lambie, D. Gao and J. Kimble, personal communication). Therefore, it has become more likely that the clr-1 phenotype is somehow related to signal transduction. We found a unique Tc1 containing DNA fragment (HindIII 2.7kb) in sma-1 let( ut102 ) unc-761 sqt-3 ,where the mutation ut102 was isolated by K. Kondo from a mut-6 strain. We are also isolating mutants that have a phenotype of incompletely penetrant clr-1 lethals. Many of them are defective also in the shape or movement of the head. For instance, ut78 IVhas a notched head (it may be an allele of vab-2 ),and ut79 IIis defective in foraging movement. Since the worms that grow to adults are not so sick, it is possible that those mutants may be mutants of cell lineage and that only those worms that adopt a lethal cell lineage may die. Anyway, we hope they will be useful in elucidating the nature of clr-1 lethals.
Katsura, Kondo and Kawase: WBG 12(2) p108 .
E. Lambie, D. Gao and J. Kimble, personal communication.