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First published online 30 September 2008
doi: 10.1242/jcs.032904

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CED-9 and mitochondrial homeostasis in C. elegans muscle

¹ Department of Biology, Johns Hopkins University, Baltimore, MD 21218, USA
² Department of Chemistry, Johns Hopkins University, Baltimore, MD 21218, USA
³ Integrated Imaging Center, Johns Hopkins University, Baltimore, MD 21218, USA
⁴ Departments of Pathology and Genetics, Stanford University SOM, Stanford, CA 94305, USA

^* Author for correspondence (e-mail: hill{at}jhu.edu)

Accepted 21 July 2008

Mitochondrial homeostasis reflects a dynamic balance between membrane fission and fusion events thought essential for mitochondrial function. We report here that altered expression of the C. elegans BCL2 homolog CED-9 affects both mitochondrial fission and fusion. Although striated muscle cells lacking CED-9 have no alteration in mitochondrial size or ultrastructure, these cells appear more sensitive to mitochondrial fragmentation. By contrast, increased CED-9 expression in these cells produces highly interconnected mitochondria. This mitochondrial phenotype is partially suppressed by increased expression of the dynamin-related GTPase DRP-1, with suppression dependent on the BH3 binding pocket of CED-9. This suppression suggests that CED-9 directly regulates DRP-1, a model supported by our finding that CED-9 activates the GTPase activity of human DRP1. Thus, CED-9 is capable of regulating the mitochondrial fission-fusion cycle but is not essential for either fission or fusion.

Key words: Bcl-2, BCL2, CED-9, DRP-1, Mitochondria, Morphology, Dynamics, Homeostasis, C. elegans, Transmembrane domain

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