Abstract
A current model for Caenorhabditis elegans vulval cell fate specification is that SynMuv genes act redundantly in the hyp7 hypodermal syncytium to repress the LIN-3/EGF inducer and prevent ectopic vulval induction of vulva precursor cells (VPCs). Here we show that the SynMuv gene hpl-2/HP1 has an additional function in VPCs, where it may act through target genes including LIN-39/Hox.
Highlights
A current model for Caenorhabditis elegans vulval cell fate specification is that synthetic multivulva (SynMuv) genes act redundantly in the hyp7 hypodermal syncytium to repress the LIN-3/epidermal growth factor (EGF) inducer and prevent ectopic vulval induction of vulva precursor cells (VPCs)
To gain insight into how hpl-2 may interact with other SynMuv genes, we investigated its cellular focus
LIN-3 is not likely to be a relevant target for HPL-2 in VPCs: Expression of a hairpin-forming lin-3 sequence in hyp7 was able to suppress the SynMuv phenotype observed for hpl-2;lin-15A mutants at 20° (Table 1)
Summary
A current model for Caenorhabditis elegans vulval cell fate specification is that SynMuv genes act redundantly in the hyp7 hypodermal syncytium to repress the LIN-3/EGF inducer and prevent ectopic vulval induction of vulva precursor cells (VPCs). Because HPL-2 is ubiquitously expressed in most cell types, including VPCs and HYP7 at all stages of development (Schott et al 2006; Figure 1), we carried out tissue-specific rescuing experiments by expressing hpl-2 cDNA under the control of the dpy-7 and lin-31 promoters, expressed in HYP7 and VPCs, respectively (Myers and Greenwald 2005).
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