How does the mammalian replisome overcome DNA protein crosslinks?

Kymograph showing how the fluorescently labelled CMG helicase (green) translocates past an intact DNA-protein crosslink (pink). From: Sparks et al. Cell 2019

Covalent DNA-protein cross-links (DPCs) impede replication fork progression and threaten genomic integrity. In two studies published in Cell and Molecular Cell Markus Räschle and colleagues identify factors which facilitate bypass and repair of these roadblocks. Using quantitative mass spectrometry, they identify an auxillary helicase, RTEL1, that helps the replisome to translocate passed the DNA lesions. Intriguingly, bypass of an intact protein DNA crosslink could directly be observed in single molecule experiments.
To identify the factors required for removal of such DNA lesions, the scientists comprehensively monitored  protein recruitment to damaged plasmids undergoing replication and repair. From the temporal profiles two proteases, SPRTN and the Proteasome, were identified to degrade the crosslinked protein from the DNA. Further mechanistic studies revealed how the protealytic activity of SPRTN and the Proteasome is controlled and activated only in the context of ongoing DNA replication. 

Kymograph showing how the fluorescently labelled CMG helicase (green) translocates past an intact DNA-protein crosslink (pink). From: Sparks et al. Cell 2019

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