lin-39

Mutations in lin-39 in Caenorhabditis elegans and Pristionchus pacificus result in a vulvaless phenotype because presumptive vulva precursor cells adopt non-vulval fates.

The Hox gene lin-39 functions downstream of both, the LIN-3/RTK/Ras pathway and LIN-1 and plays a pivotal role in controlling vulva cell competence and induction.

Mutations in lin-39 in Caenorhabditis elegans and Pristionchus pacificus result in a vulvaless phenotype because presumptive vulva precursor cells adopt non-vulval fates.

REF-2 functions with the Hox proteins to prevent Pn.p cell fusion. ref-2 may also be a transcriptional target of the Hox proteins.

C. elegans lin-39 (Cel-lin-39) indirectly controls the cell fusion gene eff-1 by regulating the GATA transcription factors egl-18 and elt-6.

During vulval induction, the Ras pathway, together with basal lin-39 activity, up-regulates lin-39 expression in vulval precursor cells.

In lin-39 mutants, mid-body cells express fates characteristic of more anterior or posterior homologs, and the migration of a neuroblast through the mid-body is defective. lin-39 acts cell autonomously in these mid-body cells and in the migrating neuroblast. lin-39 encodes a protein with an Antennapedia class homeodomain, most similar to those of the Drosophila homeotic genes Deformed and Sex combs reduced, and is located in a homeotic gene cluster with two other regional homeotic genes, mab-5 and egl-5. lin-39 and mab-5 function combinatorially in 2 ectodermal cells and have redundant functions in gonad development.

Here we identify a gene, ref-1, that regulates the hermaphrodite Pn.p cell fusion pattern largely by regulating MAB-5 activity in these cells.

C. elegans lin-39 mutants are vulvaless and the vulval precursor cells fuse with the surrounding hypodermis, whereas in P. pacificus lin-39 mutants the vulval precursor cells die by apoptosis.

C. elegans lin-39 mutants are vulvaless and the vulval precursor cells fuse with the surrounding hypodermis, whereas in P. pacificus lin-39 mutants the vulval precursor cells die by apoptosis.

Notably, mab-5 and ceh-20 are required not only during early development but also in later life stages to maintain posterior MN identity.

By characterizing three new alleles of sem-4 that we identified in a screen for vulval-defective mutants, we determined that loss of sem-4 activity results in abnormal specification of the secondary vulval cell lineages.

The Caenorhabditis elegans lin-39, mab-5 and egl-5 Hox genes specify cell fates along the anterior-posterior body axis of the nematode during postembryonic development, but little is known about Hox gene functions during embryogenesis.

Here, we show that the C. elegans labial-like gene ceh-13 is expressed in cells of many different tissues and lineages and that the rostral boundary of its expression domain is anterior to those of the other Hox genes.

In lin-39 mutants, mid-body cells express fates characteristic of more anterior or posterior homologs, and the migration of a neuroblast through the mid-body is defective. lin-39 acts cell autonomously in these mid-body cells and in the migrating neuroblast. lin-39 encodes a protein with an Antennapedia class homeodomain, most similar to those of the Drosophila homeotic genes Deformed and Sex combs reduced, and is located in a homeotic gene cluster with two other regional homeotic genes, mab-5 and egl-5. lin-39 and mab-5 function combinatorially in 2 ectodermal cells and have redundant functions in gonad development.

Down-regulation of the central hox gene lin-39 in dividing vulval cells results in their premature cell cycle exit, whereas constitutive lin-39 expression causes precocious Pn.p cell and sex myoblast divisions and prolongs the proliferative phase of the vulval cells past their normal point of arrest.

Down-regulation of the central hox gene lin-39 in dividing vulval cells results in their premature cell cycle exit, whereas constitutive lin-39 expression causes precocious Pn.p cell and sex myoblast divisions and prolongs the proliferative phase of the vulval cells past their normal point of arrest.

Using these reporters of neuronal subtype, we also find that the lin-39(ccc16) mutation disrupts neuronal fates specifically in the region where lin-39 and mab-5 are coexpressed, and that the protein encoded by lin-39(ccc16) is active only in the absence of mab-5.

We analyzed sem-4 interactions with other genes involved in vulval differentiation and determined that sem-4 does not function directly in the Ras-mediated signal transduction pathway but acts in close association with and upstream of lin-39 to promote vulval cell fate.

Here we show that LET-418, a C. elegans ortholog of the human NuRD component Mi-2, negatively modulates the activity of lin-39.