Asymmetric cell division (ACD) is a fundamental mechanism of developmental cell fate specification and adult tissue homeostasis. In C. elegans, a Wnt/beta-catenin signaling pathway regulates ACDs throughout development. Under control of Wnt ligand-induced polarity, the transcription factor TCF/POP-1 functions with Groucho family corepressors or coactivator beta-catenin/SYS-1 to repress or activate gene expression, respectively, in nascent daughter cells. To date, no Groucho phenotype has been reported in Wnt-signaled ACDs. Our initial experiments uncovered a genetic interaction between Groucho repressors and TCF/POP-1 in ACDs of the repression-dominant hypodermal stem cell lineage known as seam cells. Specifically, addition of
unc-37(RNAi) or
lsy-22(RNAi) in a
pop-1(RNAi) hypomorphic background enhances a
pop-1 loss of function phenotype. To further test this, we used null alleles of each corepressor.
unc-37(
tm4649) and
lsy-22(
ot244) nulls resulted in seam cell fate changes due to cell specification defects via symmetric divisions converting to ACDs. Additional
pop-1(RNAi) in these nulls yielded an expected increase in seam cells in the
lsy-22(
ot244) but a surprising decrease of seam cells in the
unc-37(
tm4649). Double knockdown of POP-1 and LSY-22 in the
unc-37(
tm4649) null indicate the decreased seam cell phenotype is unlikely to be a result of excess LSY-22 function, so we are testing UNC-37 for an LSY-22 independent role in regulating
pop-1 expression. Further, preliminary experiments of
lsy-22(RNAi) in the
unc-37(
tm4649) null do not show a change in seam cell fate, indicating Groucho function in the seam cells may only be observed in a TCF/POP-1 sensitized background. Conversely, in the somatic gonadal lineage,
unc-37(RNAi),
lsy-22(RNAi), or combined treatment fail to rescue the loss of signaled cell fate phenotype induced by high levels of POP-1, as expected in this activation-dominant tissue. However, double Groucho LOF results in gains of the signaled cell fate. This is the first instance of Groucho function in wildtype ACD. Together these data indicate Groucho repressor modulation of cell fate may be widespread in asymmetric cell fate decisions and suggests novel roles of individual members of the Groucho family.