A connection between the vulval and uterine lumens is required for egg laying. After the anchor cell induces vulval fates and pi fates in the vulval precursor and ventral uterine lineages, respectively, it fuses to the uterine seam (utse) cell, which is derived from the fusion of eight of the twelve pi progeny. Finally, the anchor cell nucleus moves to the distal corner of the utse, leaving the thin laminar utse process as the only obstruction between the vulval and uterine lumens. This process is believed to be broken upon initiation of egg laying, allowing a connection between the two lumens to form. In null mutants of both
cog-2/egl-13 and
lin-11, pi fate is specified, but a limited number of pi cell progeny undergo an extra division and utse nuclei fail to migrate to the proper location within the uterus (Newman et al. 1999 Development 126:5319-26, Hanna-Rose et al. 1999 Development 126:169-79), indicating utse differentiation abnormalities. As a result, the anchor cell fails to fuse to the utse cell and remains at the apex of the vulva, physically preventing egg laying.
cog-2 and
lin-11 encode Sox and LIM domain transcription factors, respectively, that are expressed in the pi lineage. The similar, though not identical, mutant phenotypes, the coinciding expression patterns and the identification of a new allele of
lin-11 in a screen for
cog-2 modifiers prompted us to examine the interaction between the two genes.
lin-11(
ps1) was identified as a mutation that caused
cog-2 null animals to burst at the vulva. Although this phenotype is no longer present after outcrossing the strain or upon the creation of the double mutant using various combinations of
cog-2 and
lin-11 alleles, the
lin-11;
cog-2 double mutant has striking abnormalities in the pi lineage that are not observed in either single mutant. Using a pi-specific, GFP marker, we observe an average of 20 and up to 32 GFP-expressing putative pi progeny in the double mutant, whereas the individual mutants display a modest increase (14) over the normal 12 pi cell progeny. We observed pi cell progeny undergoing extra divisions indicating that the GFP-positive cells result from proliferation as opposed to inappropriate fate decisions by neighboring cells. It thus appears that although
cog-2 and
lin-11 each play unique roles in utse cell fate differentiation as evidenced by their mutant phenotypes, they also have a redundant function in preventing over-proliferation of the pi lineage. We have also observed that other uterine cells whose identities have yet to be determined are mis-positioned in the double mutant and maintain or establish inappropriate close contacts with the unfused anchor cell during late stages of uterine development.