Crosstalk between SUMOylation and ubiquitylation controls DNA end resection by maintaining MRE11 homeostasis on chromatin

Tao Zhang, Han Yang, Zenan Zhou, Yongtai Bai, Jiadong Wang and Weibin Wang ()
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Tao Zhang: Peking University Health Science Center
Han Yang: Peking University Health Science Center
Zenan Zhou: Peking University Health Science Center
Yongtai Bai: Peking University Health Science Center
Jiadong Wang: Peking University Health Science Center
Weibin Wang: Peking University Health Science Center

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract DNA end resection is delicately regulated through various types of post-translational modifications to initiate homologous recombination, but the involvement of SUMOylation in this process remains incompletely understood. Here, we show that MRE11 requires SUMOylation to shield it from ubiquitin-mediated degradation when resecting damaged chromatin. Upon DSB induction, PIAS1 promotes MRE11 SUMOylation on chromatin to initiate DNA end resection. Then, MRE11 is deSUMOylated by SENP3 mainly after it has moved away from DSB sites. SENP3 deficiency results in MRE11 degradation failure and accumulation on chromatin, causing genome instability. We further show that cancer-related MRE11 mutants with impaired SUMOylation exhibit compromised DNA repair ability. Thus, we demonstrate that MRE11 SUMOylation in coordination with ubiquitylation is dynamically controlled by PIAS1 and SENP3 to facilitate DNA end resection and maintain genome stability.

Date: 2022
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DOI: 10.1038/s41467-022-32920-x

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