Diapause is an interruption in developmental progression that helps animals to survive adverse environmental conditions. However, the mechanisms that modulate developmental pathways to accommodate diapause are still unclear. In favorable conditions, C. elegans develops continuously through four larval stages. Alternatively, in unfavorable conditions, larvae enter dauer diapause after the second larval molt. One cell type that is affected by dauer is the hypodermal seam cells. Seam cells are multipotent during larval development but differentiate in adults, a process that is regulated by the heterochronic genes. Interestingly, most heterochronic genes that are required during continuous development are dispensable after dauer, suggesting that a separate developmental pathway controls post-dauer seam cell development. To shed light on such a pathway, we conducted a genetic screen for mutants displaying precocious expression of the adult-specific
col-19p::gfp marker in post-dauer larvae. In this screen we identified
ztf-16, encoding a C2H2 zinc finger transcription factor. To determine how
ztf-16 interacts with the heterochronic pathway to regulate
col-19p::gfp we did a series of epistatic experiments. The LIN-29 transcription factor directly activates
col-19 and is in turn regulated indirectly by the
let-7 microRNA. We found that the
ztf-16 precocious phenotype was epistatic to
let-7 reiterative phenotypes. Furthermore,
ztf-16::gfp expression was strongly upregulated in
let-7 mutants indicating that
ztf-16 acts downstream of
let-7. Surprisingly,
col-19p::gfp expression remained high in
lin-29(0) mutants, suggesting that
ztf-16 regulates
col-19p::gfp expression independently of
lin-29. Using RNA-seq, we found >1000 genes whose expression changes in
ztf-16(-) larvae including transcription factors that are candidate regulators of
col-19p::gfp expression. Our work describes a novel regulator of adult cell fate that functions after dauer diapause.