In C. elegans , gastrulation begins with ingression of E blastomeres at the 26-cell stage and ends with the establishment of a mature vermiform embryo 6 hours later (Sulston et al 1983). While significant research has been done on the initiation of gastrulation, ingression of cells in mid-gastrulation is not as well understood. What is clear is these later cells, derived from very distinct lineages, must acquire specific fates and positional information to ingress properly (Nance, et al 2005; Rohrschneider & Nance 2009). Using a genetic approach, my research group has been characterizing a gene important during mid-gastr ulation. We have identified
ru5 , a conditional embryonic lethal mutation that causes terminal phenotypes that include body and head enclosure failure, a detached pharynx, and other body morphogenesis defects. Temperature shift experiments indicate that the gene acts during gastrulation. The
ru5 mutation does not cause major changes in cell fate or position, as expression of six tissue-specific markers is normal. We do observe changes in the expression of
vab-7/even-skipped homeodomain protein. The defects in
vab-7 expression caused by
ru5 appear to be distinct from those caused by
tbx-8/9 mutants (Pocock, 2004; Andachi, 2004) indicating that the
ru5 allele helps to define a second regulatory pathway for
vab-7 . We have mapped the
ru5 locus to ~19 on L.G.I and are continuing experiments to identify the altered gene. We have also begun a genetic suppressor screen to identify interacting genes, using the
mos1 transposon as a mutagen (Bessereau, 2001). We wi ll report progress in these areas at the meeting.