Nuclear localization of Beclin 1 promotes radiation-induced DNA damage repair independent of autophagy

Fei Xu, Yixuan Fang, Lili Yan, Lan Xu, Suping Zhang, Yan Cao, Li Xu, Xiaoying Zhang, Jialing Xie, Gaoyue Jiang, Chaorong Ge, Ni An, Daohong Zhou, Na Yuan, Jianrong Wang

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38 Scopus citations


Beclin 1 is a well-established core mammalian autophagy protein that is embryonically indispensable and has been presumed to suppress oncogenesis via an autophagy-mediated mechanism. Here, we show that Beclin 1 is a prenatal primary cytoplasmic protein but rapidly relocated into the nucleus during postnatal development in mice. Surprisingly, deletion of beclin1 in in vitro human cells did not block an autophagy response, but attenuated the expression of several DNA double-strand break (DSB) repair proteins and formation of repair complexes, and reduced an ability to repair DNA in the cells exposed to ionizing radiation (IR). Overexpressing Beclin 1 improved the repair of IR-induced DSB, but did not restore an autophagy response in cells lacking autophagy gene Atg7, suggesting that Beclin 1 may regulate DSB repair independent of autophagy in the cells exposed to IR. Indeed, we found that Beclin 1 could directly interact with DNA topoisomerase IIβ and was recruited to the DSB sites by the interaction. These findings reveal a novel function of Beclin 1 in regulation of DNA damage repair independent of its role in autophagy particularly when the cells are under radiation insult.

Original languageEnglish (US)
Article number45385
JournalScientific reports
StatePublished - Mar 27 2017
Externally publishedYes

ASJC Scopus subject areas

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