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Caenorhabditis elegans mitofilin homologs control the morphology of mitochondrial cristae and influence reproduction and physiology
Author(s) -
Mun Ji Young,
Lee Tae Hoon,
Kim Ji Hui,
Yoo Bum Ho,
Bahk Young Yil,
Koo HyeonSook,
Han Sung Sik
Publication year - 2010
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22177
Subject(s) - crista , caenorhabditis elegans , mitochondrion , biology , microbiology and biotechnology , mitochondrial dna , inner mitochondrial membrane , mutant , mutation , genetics , gene
Human mitofilin is a mitochondrial protein that controls cristae formation. Here, we investigated the role of the Caenorhabditis elegans mitofilin homologs, IMMT‐1 and ‐2, in reproduction, physiology, and mitochondrial cristae formation. Mutation of either immt‐1 or immt‐2 produced defects in germline development and egg‐laying. These defects were exacerbated by the double mutation, which greatly reduced motility, increased levels of reactive oxygen species, decreased mitochondrial mass, and imparted resistance to oxidative stress. Cryo‐electron microscopy and electron tomography revealed that each of the single mutations resulted in curved and stacked mitochondrial crista tubules as well as a reduced number of crista junctions. The immt‐2 mutation was also associated with the presence of outer mitochondrial membrane pores, which were larger in the double mutant. IMMT‐1 and IMMT‐2 proteins were localized to the inner mitochondrial membrane, as seen by immunoelectron microscopy, and they behaved as oligomers or large complexes with F 1 F 0 ATP synthase in native polyacrylamide gel electrophoresis. These findings suggest that the two C. elegans mitofilin isoforms have non‐overlapping functions in controlling mitochondrial cristae formation. J. Cell. Physiol. 224: 748–756, 2010. © 2010 Wiley‐Liss, Inc.