Worm Breeder's Gazette 14(4): 27 (October 1, 1996)
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.
The College of Wooster, Department of Biology, Wooster, OH 44691
The tandem, cotranscribed C. elegans genes kin-15 and kin-16 encode putative transmembrane protein-tyrosine kinases (PTKs) with unusually short extracellular domains and are apparently expressed in the large hypodermal syncytium (hyp7) during larval development as this tissue expands by cell fusion (Morgan and Greenwald, 1993, Mol. Cell. Bio. 13: 7133). To further investigate the biological function of these novel PTKs in C. elegans, I have initiated a phenotypic analysis of strains carrying two Tc1-induced deletion mutations isolated by Yoshiki Andachi and Yuji Kohara (Morgan, 1995 International C. elegans Meeting). The ms12 allele is missing approximately the last five exons of kin-16, while the ms13 allele lacks most of kin-16 and the first three exons of kin-15. After performing repeated outcrosses to remove the mutator gene and any undesired mutations that may have arisen during the screens for Tc1-i! nduced mutations, each deletion mutant was linked to a nearby marker mutation (unc-4).Initially the developmental growth rate of each mutant strain was examined at 20°C (in comparison to the unc-4 control strain); in addition, the mutant strains were observed for any gross morphological abnormalities. For both mutant strains, significantly more larvae required greater than five days or never developed to adults, as compared to the unc-4 control strain (extended Tukey test, p<0.05). In addition, a significant fraction of the mutant adults extruded a gonad arm, apparently through the vulva (extended Tukey test, p<0.05).
This phenotypic analysis was repeated at 25°C to determine if greater penetrance was observed at this more restrictive temperature. Although the statistical analyses are currently inconclusive, probably due to small sample size, the preliminary results are intriguing. Each ms12 hermaphrodite produced far fewer embryos and adults than the control strain and exhibited extruded gonads much more frequently than control animals. Those ms12 embryos produced, however, became adults at essentially the same rate and frequency as the control embryos. The ms13 hermaphrodites also produced far fewer embryos and adults that the control strain; however, unlike ms12 animals, ms13 embryos and larvae more frequently grew slower at 25°C and never reached adulthood, as compared to the control strain. Future work will try to pinpoint the cellular basis of these developmental abnormalities. In particular, considering the gene expression studies, we have begun to examine the pattern of cell fusions in both mutant strains during larval development (using the MH27 monoclonal antibody).