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PNAS 108 (37): 15456-15461

Copyright © 2011 by the National Academy of Sciences.


Mitochondrial matrix Ca2+ as an intrinsic signal regulating mitochondrial motility in axons

Karen T. Changa,1, Robert F. Niescierb, and Kyung-Tai Minb,1

aZilkha Neurogenetic Institute and Department of Cell and Neurobiology, University of Southern California, Los Angeles, CA 90033; and bDepartment of Biology, Indiana University, Bloomington, IN 47405

Edited by Ronald D. Vale, University of California, San Francisco, CA, and approved August 3, 2011 (received for review April 29, 2011)

Abstract: The proper distribution of mitochondria is particularly vital for neurons because of their polarized structure and high energy demand. Mitochondria in axons constantly move in response to physiological needs, but signals that regulate mitochondrial movement are not well understood. Aside from producing ATP, Ca2+ buffering is another main function of mitochondria. Activities of many enzymes in mitochondria are also Ca2+-dependent, suggesting that intramitochondrial Ca2+ concentration is important for mitochondrial functions. Here, we report that mitochondrial motility in axons is actively regulated by mitochondrial matrix Ca2+. Ca2+ entry through the mitochondrial Ca2+ uniporter modulates mitochondrial transport, and mitochondrial Ca2+ content correlates inversely with the speed of mitochondrial movement. Furthermore, the miro1 protein plays a role in Ca2+ uptake into the mitochondria, which subsequently affects mitochondrial movement.

Author contributions: K.T.C. and K.-T.M. designed research; K.T.C. and R.F.N. performed research; K.T.C. and K.-T.M. analyzed data; and K.T.C. and K.-T.M. wrote the paper.

The authors declare no conflict of interest.

This article is a PNAS Direct Submission.

This article contains supporting information online at

1To whom correspondence may be addressed. E-mail: kyumin{at} or changkt{at}

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