Cell fusion is a ubiquitous process in C. elegans, with approximately one third of all somatic nuclei in adults found in variably sized multinucleate syncytia. In hermaphrodites, the hypodermal cells P1.p, P2.p, and P(9-11).p all fuse with
hyp7 during late L1 while P(3-8).p remain unfused and become members of the vulval equivalence group. In males, P(3-6).p and P(9-11).p remain unfused; P(9-11).p subsequently become the male equivalence group. The Pn.p fusion decision is regulated by the Hox genes
lin-39 and
mab-5.
lin-39 is expressed in P(3-8).p and in hermaphrodites prevents fusion of these cells.
mab-5 is expressed in P(7-11).p. In males,
lin-39 and
mab-5 each individually prevent Pn.p cell fusion in P(3-6).P and P(9-11).p, respectively. However, in P7.p and P8.p, where both Hox genes are expressed in the same cell, they somehow neutralize one another's effects, so that P7.p and P8.p fuse with
hyp7. We are carrying out a screen to identify additional genes that affect Pn.p cell fusion. In a
lin-12(d) background, those Pn.p cells that remain unfused all generate ectopic pseudovulvae or hooks that protrude from the ventral surface of the worm. We are screening for mutations that change the pattern of ventral protrusion in
lin-12(
n137);
him-5(
e1467); thus far, we have identified five mutants with extra ventral protrusions in the hermaphrodite and one mutant with extra protrusions in the male. MH27, a monoclonal antibody that stains adherins junctions, has been used to verify that extra Pn.p cells fail to fuse with
hyp7 in some of these mutants. Preliminary experiments suggest that some of these mutations may affect upstream regulators of the Hox genes. We also hope to find genes that integrate the Hox signals as well as genes required for the actual process of cell fusion.