The endoderm of C. elegans is clonally derived from a single progenitor, called the E cell, in the 7-cell embryo. We are studying the role of zygotic genes in specification of the endoderm. From an extensive deficiency screen ('93 Worm Meeting, p. 497) we identified a single region on LG V that appears to be required for production of an intestine. Deficiency homozygotes fail to make a differentiated gut, but produce all other major cell types. Attempts to isolate point mutations in the relevant gene(s) were unsuccessful; however, a general screen of zygotic lethal mutants yielded a single putative point mutation (
zu247). Some
zu247 animals arrest as nearly normal larvae completely lacking an intestine.
zu247 is not fully penetrant and homozygotes can be maintained as a viable strain.
zu247 appears to be cold-sensitive and appears not to be null. The fate of the E cell is altered in these mutants. Isolated E cells in
zu247 embryos and embryos homozygous for the deficiency zuDf2 produced epidermis and muscle instead of intestine, suggesting an E -> C cell fate transformation. In addition, lineage analyses of
zu247 gutless embryos at 17oC and of embryos homozygous for the deficiency itDf2 suggest that the E cell adopts a C-like lineage in these mutants. A similar E->C cell fate transformation appears to occur in
skn-1 mutants, suggesting that
end-1 might be a zygotic target of the maternal SKN-1 putative transcription factor. Surprisingly, in two
zu247 gutless embryos grown at ~23oC (a more permissive temperature) the lineage of the E cell instead strongly resembled that of MS, and excess MS-derived cells (e.g., pharynx cells) were seen in these animals. These observations suggest that the level of activity of the relevant locus may control which of three different founder cell identities, E, MS, or C, the E cell adopts. We have identified a 3.5 kb fragment that rescues the gutless phenotype of the deficiencies and
zu247, and appears to contain a single transcription unit. We refer to the rescuing activity as the
end-1 gene. Molecular analysis of
end-1 will be described.