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. 2020 Jun 25;11:839. doi: 10.3389/fpls.2020.00839

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Copyright © 2020 Yao, Li, Chen, Liu, Mi, Ren, Mo and Lu.

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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Model of ATM promote RAD51 mediated inter-sister meiotic DSB repair. After meiotic DSBs are formed, it will be processed to generated the 3’ ssDNAs (A). With the help of RAD51 and DMC1, some of the ssDNAs will invade homologous chromosomes to seek template for repair (A,B). Those DSBs repaired using homologous chromosomes will generate COs or NCOs while NCOs are in the majority (B,C). Whereas some of the DSBs are repaired through inter-sister recombination which is mediated by RAD51 (B,C). Thus, we proposed that ATM could promote this RAD51-mediated inter-sister repair process and it is possible that ATM regulate this process through phosphorylating a potential protein X (C). Thus, when ATM is absent, this inter-sister repair pathway was impaired and leads to some unrepaired meiotic DSBs which eventually result in the mild chromosome fragmentations observed in atm mutants.