The C. elegans 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, LIN-42, in C. elegans is an important regulator of developmental timing. 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 C. elegans homolog of the Drosophila Period protein kinase Doubletime. Worms containing a large deletion in
kin-20 have a significantly smaller brood size, develop slower than wild type C. elegans, and display an uncoordinated phenotype. We have previously shown that KIN-20 impacts
lin-42 phenotypes. In addition, KIN-20 is important for post-transcriptional regulation of mature
let-7 and
lin-4 microRNA expression. However, the mechanisms by which KIN-20 regulates LIN-42 and microRNA biogenesis are unclear. We have utilized CRISPR technology to generate epitope-tagged variants of LIN-42 and KIN-20 in order to further explore the relationship between these important, conserved genes and development.