The <i>Caenorhabditis elegans</i> (<i>C. elegans</i>) heterochronic pathway, which regulates developmental timing, is thought to be an ancestral form of the circadian clock in other organisms. An essential member of this clock is the Period protein whose homolog, <i>
lin-42</i>, in <i>C. elegans</i> is an important heterochronic gene. LIN-42 functions as a transcriptional repressor of multiple genes including the conserved
lin-4 and
let-7 microRNAs. Like other Period proteins, levels of LIN-42 oscillate throughout development. In other organisms this cycling is controlled in part by phosphorylation. KIN-20 is the <i>C. elegans</i> homolog of the <i>Drosophila</i> Period protein kinase Doubletime. Worms containing a large deletion in <i>
kin-20</i> have a significantly smaller brood size and develop slower than wild type <i>C. elegans</i> Here we analyze the effect of <i>
kin-20</i> on <i>
lin-42</i> phenotypes and microRNA expression. We find that <i>
kin-20</i> RNAi enhances loss-of-function <i>
lin-42</i> mutant phenotypes and that <i>
kin-20</i> mutant worms express lower levels of LIN-42. We also show that <i>
kin-20</i> is important for post-transcriptional regulation of mature
let-7 and
lin-4 microRNA expression. In addition, the increased level of
let-7 found in <i>
lin-42(
n1089)</i> mutant worms is not maintained after <i>
kin-20</i> RNAi treatment. Instead,
let-7 is further repressed when levels of <i>
kin-20</i> and <i>
lin-42</i> are both decreased. Altogether these results suggest that though <i>
kin-20</i> regulates <i>
lin-42</i> and
let-7 microRNA, it mainly affects
let-7 microRNA expression independently of <i>
lin-42</i> These findings further our understanding of the mechanisms by which these conserved circadian rhythmic genes interact to ultimately regulate rhythmic processes, developmental timing and microRNA biogenesis in <i>C. elegans</i>.