Worm Breeder's Gazette 12(2): 108 (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 isolated and characterized twenty-three mutants of C. elegans that die as abnormal-shaped larvae. We think they will be useful in studies on the essential genes and functions in late embryonic and early post-embryonic development. Those mutants that we regarded as abnormal-shaped form 5 to 10 X of the total larval lethal mutants. At least eight of them are located in known genes. The twenty-three mutants were classified into six categories by gross morphology [See Figure 1]. They were studied further by Nomarski microscopy and by fluorescence microscopy combined with staining by DAPI and by rhodamine-phalloidine. Furthermore, we have also characterized four incompletely penetrant lethal and one viable mutations isolated in the same screen. They were classified into four categories, and three of them have been mapped in known genes. All the mutants that have coiled and 4-fold shape are related to neuron and muscle, respectively. They were mapped to known genes except ut36 ,which we are asking Drs. B. Williams and R. Waterston to test whether they map in pat-2 .As expected, there are many mutants that seem to be defective in cuticle or hypodermis ((1),(2),(7),(8) and (9) in the Table). However, in spite of being classified in (1), ut39 may be defective in the body elongation rather than the cuticle, since it appears to stop development at 2-fold stage, as judged from the anterior location of some nuclei and the widely open anus. Mutants of category (3) are only slightly different from wild type worms in the outer shape. However, one of them, ut45 ,is abnormal in the shape of intestine cells. We plan to isolate more mutants of such phenotype. Probably the most striking result of this study is that there are many mutants of the clr-1 phenotype, that is, mutants in which the outer surface of the intestine is gradually detached from the inner surface of the body wall during larval growth. One of them maps in clr-1 ,which exceptionally grows into a sterile, dumpy adult. Unlike the known allele e1745 it is not temperature-sensitive. The other mutants having the clr-1 phenotype do not map in clr-1 and die at L1 or L2 .Since one of them maps in let-23 ,we are testing if the lethality of other mutants are suppressed by lin-1 (cf. Clark & Horvitz: WBG 10(3) p134 ),expecting that some of them may have a role in signal transduction pathways.
The alleles having numbers lower than 100 were mutagenized by EMS, and higher than 100 by mut-6 .The gene names without parentheses show the genes in which the mutations are located. They were assigned by complementation tests with known mutations except for mup-1 and hch-1 ,which were assigned only by the location and the phenotype. The gene names in parentheses are genes near the mutations and usually not the genes themselves where the mutations are located.