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. 2021 Apr 15;9:669041. doi: 10.3389/fcell.2021.669041

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Copyright © 2021 da Silva.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic overview of the possible trypanosomatid cell’s fate in response to DNA double-strand breaks (DSBs). In a hypothetical trypanosomatid, several players act in an orchestrated way in response to DSBs. However, according to the number, location, cell cycle phase, and DNA repair capacity of the cell, these lesions can trigger different consequences: advantages (green box), neutrality (gray box), or disadvantages (red box). ATM, ataxia telangiectasia mutated; ATR, ataxia telangiectasia and Rad3-related; MRN, MRE11-RAD50-NBS1 complex; Exo1, Exonuclease 1; RPA, Replication protein A; BRCA1-2, Breast cancer 1–2; Rad51, Recombinase involved in homologous recombination; γH2A, phosphorylated histone H2A.