The highly conserved Dp, Retinoblastoma-like, E2F, and MuvB (DREAM) transcriptional repressor complex is best known as a negative regulator of cell cycle progression. We previously established that the 5-subunit MuvB complex innately functions as the mediator of DRM target gene repression in Caenorhabditis elegans. How the DREAM complex mediates transcriptional repression remains an outstanding question, primarily because MuvB complex activity is required for viability, limiting the utility of mutational analyses. To overcome such limitations, we are utilizing the Auxin-Inducible Degron (AID) system to precisely and rapidly degrade MuvB subcomplex components in C. elegans. Using CRISPR/Cas9-mediated genomic editing, we degron-tagged two key MuvB components,
lin-9 and
lin-54, and crossed each into a transgenic strain expressing the Arabidopsis thaliana TIR1 E3 ubiquitin ligase in somatic cells. We expected that auxin-induced degradation of either LIN-9, which we hypothesize functions as a core structural component of MuvB, or LIN-54, which acts as the sole DNA-binding component in MuvB, would lead to upregulation of DREAM target genes. Interestingly, we observed that degradation of the LIN-54 but not LIN-9 caused upregulation of DREAM target genes within a 6-hour auxin treatment timecourse in L1 larvae. Our results suggest that MuvB chromatin localization mediated by LIN-54 is critical for DREAM target gene repression. These studies lay the foundation for future degron-mediated analyses assessing DREAM complex function.