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First published online 1 November 2005
doi: 10.1242/jcs.02645

Journal of Cell Science 118, 5357-5367 (2005)
Published by The Company of Biologists 2005
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Research Article

MIDAS/GPP34, a nuclear gene product, regulates total mitochondrial mass in response to mitochondrial dysfunction

Naomi Nakashima-Kamimura1, Sadamitsu Asoh1, Yoshitomo Ishibashi1, Yuri Mukai1,*, Yujiro Shidara1,2, Hideaki Oda2, Kae Munakata3, Yu-ichi Goto3 and Shigeo Ohta1,{ddagger}

1 Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, 1-396 Kosugi-cho, Kawasaki, Kanagawa, 211-8533, Japan
2 Department of Pathology, Tokyo Women's Medical University, School of Medicine, Shinjuku-ku, Tokyo, 162-8666, Japan
3 Department of Mental Retardation and Birth Defect Research, National Institute of Neuroscience, NCNP, Kodaira, Tokyo, 187-8502, Japan

{ddagger} Author for correspondence (e-mail:ohta{at}nms.ac.jp)

Accepted 15 August 2005

To investigate the regulatory system in mitochondrial biogenesis involving crosstalk between the mitochondria and nucleus, we found a factor named MIDAS (mitochondrial DNA absence sensitive factor) whose expression was enhanced by the absence of mitochondrial DNA (mtDNA). In patients with mitochondrial diseases, MIDAS expression was increased only in dysfunctional muscle fibers. A majority of MIDAS localized to mitochondria with a small fraction in the Golgi apparatus in HeLa cells. To investigate the function of MIDAS, we stably transfected HeLa cells with an expression vector carrying MIDAS cDNA or siRNA. Cells expressing the MIDAS protein and the siRNA constitutively showed an increase and decrease in the total mass of mitochondria, respectively, accompanying the regulation of a mitochondria-specific phospholipid, cardiolipin. In contrast, amounts of the mitochondrial DNA, RNA and proteins did not depend upon MIDAS. Thus, MIDAS is involved in the regulation of mitochondrial lipids, leading to increases of total mitochondrial mass in response to mitochondrial dysfunction.

Key words: Mitochondria, Mitochondrial mass, Cardiolipin, Mitochondrial DNA, Mitochondrial disease, Golgi apparatus




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