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FA is produced from several exogenous and endogenous sources and has been linked to many cancer types. Persistent adducts are often bypassed by error-prone translesion synthesis (TLS) polymerases, causing mutations that contribute to the FA-induced mutational spectrum. However, it is unknown how DPC repair and TLS coordinate to bypass FA damage, and how bypass by different TLS polymerases alters FA\u2019s mutational spectrum. Here, we use an established yeast mutational reporter system to confirm that FA preferentially mutagenizes guanine residues within single-stranded\u00a0DNA (ssDNA). We find that functional TLS prevents chromosomal instability following FA exposure and that FA-induced chromosomal rearrangements are dependent on DPC repair. Finally, we find that the TLS polymerases Rev1 and Pol \u03b7 function together to prevent FA mutagenesis. Overall, these results outline the mechanisms by which TLS and DPC repair coordinate to bypass FA-induced ssDNA damage.<\/jats:p>","DOI":"10.1093\/nar\/gkaf914","type":"journal-article","created":{"date-parts":[[2025,9,3]],"date-time":"2025-09-03T11:42:07Z","timestamp":1756899727000},"source":"Crossref","is-referenced-by-count":5,"title":["Translesion polymerases and DNA\u2013protein crosslink repair shapes the cellular response to formaldehyde-induced DNA damage in ssDNA"],"prefix":"10.1093","volume":"53","author":[{"given":"Thomas","family":"Blouin","sequence":"first","affiliation":[{"name":"Medical University of South Carolina Department of Biochemistry and Molecular Biology, , Charleston, SC 29425 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Ampolini","sequence":"additional","affiliation":[{"name":"Medical University of South Carolina Department of Biochemistry and Molecular Biology, , Charleston, SC 29425 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