The C. elegans heterochronic pathway is composed of multiple proteins and microRNAs that regulate developmental timing. microRNAs are ~22 nucleotide RNAs that post-transcriptionally silence gene expression, and are thus essential in diverse biological processes. Previous work in our lab and others has shown that the heterochronic pathway member and circadian rhythm Period protein homolog, LIN-42, regulates microRNA biogenesis. Like other period proteins, levels of LIN-42 oscillate throughout development. In other organisms this cycling is controlled in part by phosphorylation and dephosphorylation events. KIN-20 is the C. elegans homolog of the D. melanogaster Period protein kinase doubletime. Worms containing a large deletion in kin-20 develop slower and have a significantly smaller brood size than wild type C. elegans. Here we analyze the effect of KIN-20 on the expression of the canonical heterochronic miRNAs let-7 and lin-4. We find that let-7 and lin-4 levels are significantly decreased and that mRNA levels of the let-7 target lin-41 are increased in kin-20 mutant worms relative to wild type. Additionally, we find that primary let-7 and primary lin-4 levels are unchanged in kin-20 mutant worms suggesting that KIN-20 impacts miRNA biogenesis downstream of miRNA transcription. Current work seeks to determine if these effects are dependent on LIN-42. To further explore the relationship of KIN-20 and LIN-42, we analyzed the effect of KIN-20 on endogenous LIN-42 expression. Based on the homologous system in D. melanogaster, we hypothesized that KIN-20 phosphorylates LIN-42 to trigger LIN-42 degradation. Surprisingly, we find that KIN-20 effects on LIN-42 differ depending on the isoform analyzed. Altogether these results help uncover the mechanisms by which these conserved circadian rhythmic genes interact to ultimately regulate rhythmic processes, developmental timing and microRNA biogenesis in C. elegans.