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We discovered that collaboration between TOP1 and the BER pathway can substitute for the lack of NER. This previously unappreciated repair pathway is initiated by TOP1-dependent sensing topological alterations near UV lesions and subsequent SSB formation followed by BER. Considering that the SSB formation by TOP1 is the rate-limiting step, and TOP1 expression is very low in the skin and neuronal tissues, our finding may help understand the molecular mechanisms and genetic determinants underlying the neurological dysfunction of XP patients, although TOP1-relevant endogenous lesions are currently unknown.<\/jats:p>","DOI":"10.1073\/pnas.1920165117","type":"journal-article","created":{"date-parts":[[2020,6,8]],"date-time":"2020-06-08T20:32:11Z","timestamp":1591648331000},"page":"14412-14420","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":35,"title":["Topoisomerase I-driven repair of UV-induced damage in NER-deficient cells"],"prefix":"10.1073","volume":"117","author":[{"given":"Liton Kumar","family":"Saha","sequence":"first","affiliation":[{"name":"Department of Radiation Genetics, Kyoto University, Graduate School of Medicine, 606-8501 Kyoto, Japan;"},{"name":"Developmental Therapeutics Branch and 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