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Fis1, Mff, MiD49, and MiD51 mediate Drp1 recruitment in mitochondrial fission

Losón, Oliver C. and Song, Zhiyin and Chen, Hsiuchen and Chan, David C. (2013) Fis1, Mff, MiD49, and MiD51 mediate Drp1 recruitment in mitochondrial fission. Molecular Biology of the Cell, 24 (5). pp. 659-667. ISSN 1059-1524. PMCID PMC3583668. doi:10.1091/mbc.E12-10-0721.

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Several mitochondrial outer membrane proteins—mitochondrial fission protein 1 (Fis1), mitochondrial fission factor (Mff), mitochondrial dynamics proteins of 49 and 51 kDa (MiD49 and MiD51, respectively)—have been proposed to promote mitochondrial fission by recruiting the GTPase dynamin-related protein 1 (Drp1), but fundamental issues remain concerning their function. A recent study supported such a role for Mff but not for Fis1. In addition, it is unclear whether MiD49 and MiD51 activate or inhibit fission, because their overexpression causes extensive mitochondrial elongation. It is also unknown whether these proteins can act in the absence of one another to mediate fission. Using Fis1-null, Mff-null, and Fis1/Mff-null cells, we show that both Fis1 and Mff have roles in mitochondrial fission. Moreover, immunofluorescence analysis of Drp1 suggests that Fis1 and Mff are important for the number and size of Drp1 puncta on mitochondria. Finally, we find that either MiD49 or MiD51 can mediate Drp1 recruitment and mitochondrial fission in the absence of Fis1 and Mff. These results demonstrate that multiple receptors can recruit Drp1 to mediate mitochondrial fission.

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Chan, David C.0000-0002-0191-2154
Additional Information:© 2013 Losón et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License ( Received: Oct 9, 2012; Revised: Dec 13, 2012; Accepted: Dec 21, 2012. This article was published online ahead of print in MBoC in Press ( on January 2, 2013. This work was supported by the National Institutes of Health (GM062967). O.C.L. was supported by an R. L. Kirschstein National Research Service Award (5F31GM089327). The Drp1-null cells were a generous gift from Katsuyoshi Mihara (Kyushu University, Fukuoka, Japan).
Funding AgencyGrant Number
NIH Predoctoral Fellowship5F31GM089327
Issue or Number:5
PubMed Central ID:PMC3583668
Record Number:CaltechAUTHORS:20130722-112639794
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:39495
Deposited By: Tony Diaz
Deposited On:22 Jul 2013 20:55
Last Modified:09 Nov 2021 23:45

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