The ATM–BID pathway plays a critical role in the DNA damage response by regulating mitochondria metabolism

Dear Editor,

We are writing this correspondence as an attempt to resolve controversy in the field regarding the role of BID in the DNA damage response (DDR). BID is a well-established BH3-only BCL-2 family member that has a critical role in regulating mitochondrial apoptosis.¹ Previously we have reported that DNA damage induces the phosphorylation of BID on serines 61 and 78 by the ataxia-telangiectasia mutated (ATM) kinase, and that this phosphorylation is important for cell cycle arrest and inhibition of apoptosis.² In addition, another group reported similar results in response to replicative stress.³ Nevertheless, these findings were challenged by a third group, which demonstrated that in response to DNA damage BID^−/− cells underwent cell cycle arrest and apoptosis in a manner indistinguishable from wild-type cells, arguing that BID is dispensable for the DDR.⁴ This study did not however touch upon the connection between BID and ATM. Thus, the role of BID in the DDR in the minds of many was not resolved.

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