HPL-2/HP1 prevents inappropriate vulval induction in Caenorhabditis elegans by acting in both HYP7 and vulval precursor cells.

HPL-2/HP1 prevents inappropriate vulval induction in C. elegans by acting in both HYP7 and Vulval Precursor Cells

The C. elegans HP1 homologue HPL-2 and the LIN-13 zinc finger protein form a complex implicated in vulval development.

HP1 proteins are essential components of heterochromatin and contribute to the transcriptional repression of euchromatic genes via the recruitment to specific promoters by corepressor proteins including TIF1 and Rb. The Caenorhabditis elegans HP1 homologue HPL-2 acts in the "synMuv" (synthetic multivulval) pathway, which defines redundant negative regulators of a Ras signaling cascade required ...

A heterochromatin protein 1 homologue in Caenorhabditis elegans acts in germline and vulval development.

Proteins of the highly conserved heterochromatin protein 1 (HP1) family have been found to function in the dynamic organization of nuclear architecture and in gene regulation throughout the eukaryotic kingdom. In addition to being key players in heterochromatin-mediated gene silencing, HP1 proteins may also contribute to the transcriptional repression of euchromatic genes via the recruitment to...

Wnt signal from multiple tissues and lin-3/EGF signal from the gonad maintain vulval precursor cell competence in Caenorhabditis elegans.

The Caenorhabditis elegans vulva has been a valuable paradigm for defining components of signaling pathways and elucidating how signaling events are coordinated to generate a developmental pattern. Vulval precursor cells (VPCs) are induced to adopt vulval fates in the third larval stage by LIN-3, an EGF-like signal produced by the gonad. Competence to respond to the inductive signal requires th...

A gonad-derived survival signal for vulval precursor cells in two nematode species

Intercellular cell-survival signals play a major role in animal development [1]. In the nematode Caenorhabditis elegans, however, the stereotyped cell deaths that occur reproducibly during development are regulated in a cell-autonomous fashion (or, in a few cases, by a death-inducing signal) [2]. We show here the existence of a cell-survival signal acting on the vulval precursor cells in two ne...