Apaf‐1 localization is modulated indirectly by Bcl‐2 expression

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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.