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First published online October 8, 2008

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CED-9: moulding mitochondria?

The morphology of mitochondria impacts on their function and is highly dynamic - mitochondria can undergo fission (to become fragmented) and fusion (to form an interconnected network). The proteins of the BCL2 family, which regulate apoptosis, have been proposed to modulate mitochondrial morphology by interacting with large GTPases such as DRP-1 and mitofusin (which control fission and fusion, respectively) - but how important is their role? To address this question, R. Blake Hill and colleagues (p. 3373) investigate the effect of CED-9 (the sole BCL2 homologue in C. elegans) on mitochondrial homeostasis. The authors show that in worms carrying ced-9 loss-of-function mutations, mitochondrial morphology in muscle cells is grossly normal, but worms that lack CED-9 are more prone to DRP-1-induced mitochondrial fragmentation than those expressing the wild-type protein. By contrast, increasing CED-9 expression leads to highly interconnected mitochondria; this phenotype is partially suppressed by the increased expression of DRP-1, and is dependent on the BH3-binding domain of CED-9. Thus, although CED-9 is not essential for either fission or fusion, it can regulate both processes. This increases our understanding of the interplay between BCL2 proteins and mitochondrial morphology.

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Related articles in JCS:

CED-9 and mitochondrial homeostasis in C. elegans muscle

Frederick J. Tan, Michelle Husain, Cara Marie Manlandro, Marijke Koppenol, Andrew Z. Fire, and R. Blake Hill
JCS 2008 121: 3373-3382. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?