Worm Breeder's Gazette 13(3): 32 (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.


Bruce Bowerman, Paula R. Martin, Christopher J. Thorpe, Christopher A. Shelton

The Institute of Molecular Biology, University of Oregon, Eugene, OR 97403.

During a screen for recessive, maternal-effect, embryonic-lethal mutations, we recovered six strains in which homozygous mutant mothers produce embryos that phentoypically resemble skn-1 mutant embryos. They appear to lack both pharyngeal and intestinal cells, normally made by the ventral-most 4-cell stage blastomere EMS, and instead make extra hypodermal cells. Three of the strains proved to carry mutant alleles of the skn-1 gene ( or12 , or13 ,and or19 )on chromosome IV. However, the other three strains carry allelic mutations ( or16 , or17 ,and or27 )in another maternal gene we currently call skn-4 ,near unc-47 on chromosome III.

Mutations in skn-1 result in EMS adopting a fate more like that of its sister, P2 (Bowerman et al. Cell 68, 1061-1075). Preliminary results indicate that mutations in skn-4 cause a similar phenotype: EMS produces hypodermal and body wall muscle cells instead of pharynx and intestine, while other blastomeres appear to develop normally. Although similar, the Skn-1 and Skn-4 mutant phenotypes also differ in one intriguing way. While mutations in skn-1 more severely affect the fate of one EMS daughter called MS, mutations in skn-4 more severely affect the fate of the other daughter, E. For example, strong alleles of skn-1 result in 99% of mutant embryos lacking MS-derived pharyngeal cells, but only 80% lack E-derived intestinal cells. In contrast, only 50% of skn-4 mutant embryos completely lack pharyngeal cells (80% lack all but a few pharyngeal cells), but 90-95% fail to produce intestinal cells. Double mutant, skn-4 ; skn-1 embryos, show an additive phenotype: neither pharyngeal or intestinal cells are made in most embryos, and other blastomeres appear to develop normally. Our analysis suggests that skn-4 may be required together with skn-1 to specify EMS fate. The divergent developmental pathways of the two EMS daughters may therefore require genes with overlapping but distinct functions. The identification of additional genes that mutate to give a Skn-like phenotype raises a variety of issues concerning the possible involvement of additional localized (or unlocalized) factors in the specification of EMS fate.