In C. elegans, all endoderm originates from one 8-cell stage blastomere called E. E and its sister, MS, a mesodermal precursor, are the daughters of EMS, a 4-cell stage blastomere. A neighboring 4-cell stage blastomere called P2 sends a signal to EMS that is required for the specification of E fate; when the P2 signal is disrupted, both EMS daughters develop like MS, producing extra mesoderm but no endoderm (B. Goldstein, 1992,1995). To study this inductive specification of E fate, we have identified 13 recessive, maternal-effect mutations that result in a lack of endoderm and an excess of mesoderm. These mutants, that we call mom for more mesoderm, define 4 genes,
mom-1, 2, 3 & 4.
mom-1 on LGX and
mom-2 on LGV (5 alleles of each) are required in P2 to signal EMS (see abstract by Chris Thorpe). More recently, we have found one allele of
mom-3 on LGII and two alleles of
mom-4 on LGI. The penetrance of the endoderm defect varies from 50 to 80% for
mom-1 alleles, from 15 to 85% for
mom-2 alleles, and is 8% and 42% for the two alleles of
mom-4 . 75% of
mom-3 mutant embryos lack endoderm and produce excess mesodermal cell types, such as pharyngeal muscle cells. As shown by laser ablation experiments, the excess mesoderm in
mom-3 mutants is derived from E: approximately 70% of isolated
mom-3 mutant E blastomeres produce pharyngeal cells but no endodermal intestinal cells. Preliminary lineage analysis shows that E in
mom-3 mutant embryos divides early, with a timing similar to the division of MS. These results support the hypothesis that E adopts an MS-like fate in
mom-3 mutants. We also will determine if
mom-3 function is required for the induction of endoderm, either for sending or receiving the P2 signal that specifies E fate.