In both Caenorhabditis elegans and Pristionchus pacificus, the vulva occupies the mid-body region and is formed from the differentiation of ventral epidermal cells. Both species also require the function of the homeobox gene
lin-39 for vulval development, since
lin-39 mutants are vulvaless and all vulval precursor cells adopt the fates of their anterior and posterior neighbors. However, while
Cel-lin-39prevents cell fusion in the vulval precursor cells,
Ppa-lin-39 prevents programmed cell death in the corresponding cells. Furthermore,
Ppa-lin-39 is required only for the initial patterning of vulval precursor cells, but does not play an instructive role in the later step of vulval specification1. The
Ppa-ced-3 mutation defective in carrying out cell death can fully rescue the vulvaless
Ppa-lin-39 mutant phenotype. What accounts for the divergence of
lin-39 function in these two nematodes? Since the Ppa-LIN-39 protein can rescue
Cel-lin-39 mutants2, differences in
lin-39 targets may account for the changes in function- either by changing
Ppa-lin-39s expression pattern or by Ppa-LIN-39 acting with co-activators synergistically. Such changes could co-opt the use of existing cell fate pathways, such as programmed cell death. Caspase-mediated cell death pathways appear highly conserved, hence developmental regulators such as LIN-39 may have evolved to tap in (or out) of this pathway to confer new cell fates. For example, in the ventral epidermal lineage, both the VC neuroblast sister cells (P(1-2,9-12).aap) in C.elegans as well as the non-vulval Pn.p cells (P(1-4,9-11).p) in P.pacificus undergo
ced-3 dependent cell death1,3. To investigate the possibility that Ppa-LIN-39 has anti-apoptotic function, we sought to construct an in vivo assay for the prevention of the
ced-3 mediated programmed cell death in hermaphrodite-specific neurons (HSNs) of C.elegans males, where endogenous
lin-39 is not expressed. By expressing
Ppa-lin-39 and its interacting partners in an artificial, HSN-specific manner, we can determine whether or not Ppa-LIN-39, either on its own or with co-activators, can prevent apoptosis in HSNs. 1.Sommer, R. J. et al. The Pristionchus HOX gene
Ppa-lin-39 inhibits programmed cell death to specify the vulva equivalence group and is not required during vulval induction. Development (Cambridge) 125, 3865-3873 (1998). 2.Grandien, K. & Sommer, R. J. Functional comparison of the nematode Hox gene
lin-39 in C. elegans and P. pacificus reveals evolutionary conservation of protein function despite divergence of primary sequences. Genes Dev 15, 2161-72. (2001).