Tissue-specific stem cells maintain the ability to produce multiple cell types during long periods of non-division, or quiescence. Similarly, in C. elegans dauer larvae, progenitor cells are quiescent and maintain the ability to produce all normal cell types after dauer. Indeed, a process involving
daf-16 actively re-establishes multipotent cell fate in vulval precursor cells during dauer. Here, we examine the role of
daf-16 in a different progenitor cell type, lateral hypodermal seam cells. Seam cells are multipotent in larvae but differentiate at adulthood. We found that
daf-16(0) dauer larvae expressed multiple endogenous adult-specific collagens as well as the adult cell-fate marker,
col-19p::gfp, thus linking
daf-16 to seam cell multipotency. During continuous development,
col-19 expression is directly activated by the LIN-29 transcription factor.
lin-29 is in turn directly repressed by the LIN-41 RNA-binding protein. We found that
lin-41 also regulates
col-19 during dauer because
lin-41(RNAi) dauer larvae expressed
col-19p::gfp.
daf-16 appears to act upstream of
lin-41 because
lin-41 expression was reduced in
daf-16(0) dauer larvae. Furthermore, a
lin-41 gain-of-function allele suppressed the
col-19p::gfp phenotype in
daf-16(RNAi) dauer larvae. Surprisingly, our data suggest that
lin-29 plays a minor role in regulating
col-19p::gfp expression during dauer. Loss of
lin-29 did not completely suppress the precocious
col-19p::gfp phenotype observed in
lin-41(-) dauer larvae. In addition, loss of
lin-29 had no effect on the
col-19p::gfp phenotype in
daf-16(0) dauers, and expression of an endogenously tagged
lin-29::gfp was unaffected in
daf-16(0) dauer larvae. Taken together, our data suggest that
col-19p::gfp expression during dauer is regulated at least partially independently of
lin-29. We used RNA-seq to identify other potential regulators of
col-19p::gfp during dauer and found over 3000 genes that are differentially expressed at least 2-fold (FDR < 0.05) in
daf-16(0) vs. control dauers, including over 200 transcription factors. This work demonstrates that
daf-16 coordinates dauer formation with seam cell fate via a novel mechanism. This mechanism may be conserved in mammals where the
daf-16 ortholog, FOXO is essential for both quiescence and stem cell maintenance.