By the 4-cell stage of C. elegans embryogenesis, a ventral blastomere, called EMS, is already committed to producing pharyngeal and intestinal cell types. Recessive, maternal-effect mutations in the gene skn-1 prevent EMS from producing both pharyngeal and intestinal cells. In skn-1 mutant embryos, EMS instead produces hypodermal cells and body wall muscle cells, much like its sister blastomere. Genetic analysis suggests that the skn-1 gene product is also required required post-embryonically for development of the intestine. We have cloned and sequenced the skn-1 gene and describe sequence similarities to the basic regions of bZIP transcription factors. We propose that the maternally expressed skn-1 gene product acts to specify the fate of the EMS blastomere.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)