Apaf-1 localization is modulated indirectly by Bcl-2 expression.

ABSTRACT

Apoptotic protease activating factor-1 (Apaf-1) is an adaptor molecule essential for caspase-9 activation. Subcellular analysis of Apaf-1 in NIH-3T3 fibroblasts and the immature murine B cell lymphoma WEHI-231 indicates that Apaf-1 is localized in the Golgi apparatus and cytoplasm. Bcl-2 overexpression in WEHI-231 cells disrupts Apaf-1 localization in Golgi, causing a perinuclear Apaf-1 redistribution. Bcl-2 overexpression in NIH-3T3 fibroblasts however does not cause similar Apaf-1 redistribution, suggesting that cell type factors are involved in the redistribution process. The ability of Bcl-2 to modify Apaf-1 subcellular localization is not explained by direct interaction between Apaf-1 and Bcl-2. These data may help to clarify the anti-apoptotic Bcl-2 function.