Journal: Progress in biophysics and molecular biology
Article Title: Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes
doi: 10.1016/j.pbiomolbio.2020.08.005
Figure Lengend Snippet: Function of Hrq1 and Pso2 in ICL repair and consequences of their deletion. Following NER-induced incisions on either side of the ICL (red line), Hrq1 (blue) and Pso2 (orange) are recruited to digest one strand of DNA between the incisions. In the absence of Hrq1, Pso2 retains minimal translesional nuclease activity, so some lesions persist. In the absence of Pso2, alternative repair machinery can be recruited to repair the lesion, but most ICLs persist and lead to cell death.
Article Snippet: However, previous work with Pso2 did not demonstrate translesion nuclease activity ( Tiefenbach and Junop, 2012 ), suggesting that an accessory factor is required to promote digestion through the lesion.
Techniques: Activity Assay