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Bcl-2 family proteins reorganize mitochondrial membranes during apoptosis, to form pores and rearrange cristae. In vitro and in vivo analysis integrated with human genetics reveals a novel homeostatic mitochondrial function for Bcl-2 family protein Bid. Loss of full-length Bid results in apoptosis-independent, irregular cristae with decreased respiration.  Bid-/-  mice display stress-induced myocardial dysfunction and damage. A gene-based approach applied to a biobank, validated in two independent GWAS studies, reveals that decreased genetically determined BID expression associates with myocardial infarction (MI) susceptibility. Patients in the bottom 5% of the expression distribution exhibit &gt;4 fold increased MI risk. Carrier status with nonsynonymous variation in Bid’s membrane binding domain, Bid M148T , associates with MI predisposition. Furthermore, Bid but not Bid M148T  associates with Mcl-1 Matrix , previously implicated in cristae stability; decreased MCL-1 expression associates with MI. Our results identify a role for Bid in homeostatic mitochondrial cristae reorganization, that we link to human cardiac disease.

Bid maintains mitochondrial cristae structure and function and protects against cardiac disease in an integrative genomics study