Journal
JOURNAL OF CELL BIOLOGY
Volume 167, Issue 4, Pages 661-672Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200406038
Keywords
-
Categories
Funding
- NIDDK NIH HHS [R01 DK51526, R01 DK051526] Funding Source: Medline
Ask authors/readers for more resources
Mitochondria are dynamic organelles in cells. The control of mitochondrial motility by signaling mechanisms and the significance of rapid changes in motility remains elusive. In cardiac myoblasts, mitochondria were observed close to the microtubular array and displayed both short- and long-range movements along microtubules. By clamping cytoplasmic [Ca2+] ([Ca2+](c) at various levels mitochondrial motility was found to be regulated by Ca2+ in the physiological range. Maximal movement was obtained at resting [Ca2+](c) with complete arrest at 1-2 muM. Movement was fully recovered by returning to resting [Ca2+](c), and inhibition could be repeated with no apparent desensitization. The inositol 1,4,5-trisphosphate- or ryanodine receptor-mediated [Ca2+](c) signal also induced a decrease in mitochondrial motility. This decrease followed the spatial and temporal pattern of the [Ca2+], signal. Diminished mitochondrial motility in the region of the [Ca2+](c) rise promotes recruitment of mitochondria to enhance local Ca2+ buffering and energy supply. This mechanism may provide a novel homeostatic circuit in calcium signaling.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available