A Novel UV Resistance in Rad23-Depleted Tetrahymena thermophila

Rad23 is a highly conserved cellular scaffold protein which participates in the nucleotide excision repair pathway and ubiquitin proteasome system. It is hypothesized that the contradictory roles of Rad23 within these two systems, acting to enhance stability or facilitate degradation respectively, could be regulated via post-translational modification of the ubiquitin-like domain of the protein. To this end, a Rad23 somatic knockout cell line was established in Tetrahymena thermophila, with the eventual goal of knocking in a mutant Rad23 protein lacking potential for UbL ubiquitylation. In contrast to the UV-sensitive phenotype observed in similar models, Rad23-depleted Tetrahymena cell lines displayed significantly increased resistance to UV irradiation. While the mechanism of this survivability remains poorly understood, this model may shed new light on potential compensatory DNA repair mechanisms, pathways of failed apoptotic induction, or additional novel roles of the Rad23 accessory protein that have yet to be explored