Search bioRxiv⌕ Search

Biology subjects

Roddan, R.

Publications and source records attributed to Roddan, R..

2 recordsLinked to original sources

The dual ubiquitin binding mode of SPRTN secures rapid spatiotemporal proteolysis of DNA-protein crosslinks

DNA-protein crosslinks (DPCs) are endogenous and chemotherapy-induced genotoxic DNA lesions and, if not repaired, lead to embryonic lethality, neurodegeneration, premature ageing, and cancer. DPCs are heavily polyubiquitinated, and the SPRTN protease and 26S proteasome emerged as two central enzymes for DPC proteolysis. The proteasome recognises its substrates by their ubiquitination status. How SPRTN protease, an essential enzyme for DPC proteolysis, achieves specificity for DPCs still needs to be discovered. We found that the N-terminal SPRTN catalytic region (SprT) possesses a ubiquitin-binding domain named the Ubiquitin interface of SprT Domain (USD). Using multiple biochemical, biophysical, and structural approaches, we reveal that USD binds ubiquitin chains. SPRTN binding to ubiquitin chains via USD leads to [~] 67-fold higher activation of SPRTN proteolysis towards polyubiquitinated DPCs than the unmodified DPCs. This study reveals the ubiquitination of DPCs is the key signal for SPRTNs substrate specificity and rapid proteolysis.

biochemistry↗

Molecular insights into the stimulation of SNM1A nuclease activity by CSB during interstrand crosslink processing

The Cockayne Syndrome B (CSB, ERCC6) protein, interacts with the exonuclease SNM1A during transcription-coupled DNA interstrand (ICL) repair, with CSB facilitating localisation of SNM1A to ICL damage. The functional and mechanistic details of this interaction in DNA repair, however, have not been defined. Here, we demonstrate that CSB enhances SNM1A resection through ICLs and identify a specific interaction between the winged-helix domain of CSB and the nuclease core of SNM1A that is crucial for recruitment and enhancement of nuclease degradation. Biochemical and single-molecule studies on DNA containing site-specific ICLs reveal that CSB increases the affinity of SNM1A to damaged DNA substrates and also alters the substrate conformation to enhance ICL processing by SNM1A. Notably, CSB was observed preferentially as a dimer when colocalised with SNM1A at ICLs, constrasting with its monomeric nature observed during repair initiation in classical transcription-coupled nucleotide excision repair. The combined results provide molecular insights into the basis of a direct contribution of CSB to a DNA repair reaction.

biochemistry↗