Cited 6 time in webofscience Cited 8 time in scopus

Dynamin-related protein 1 controls the migration and neuronal differentiation of subventricular zone-derived neural progenitor cells

Title
Dynamin-related protein 1 controls the migration and neuronal differentiation of subventricular zone-derived neural progenitor cells
Authors
Kim, HJ[Kim, Hyun Jung]Shaker, MR[Shaker, Mohammed R.]Cho, B[Cho, Bongki]Cho, HM[Cho, Hyo Min]Kim, H[Kim, Hyun]Kim, JY[Kim, Joo Yeon]Sun, W[Sun, Woong]
DGIST Authors
Cho, B[Cho, Bongki]
Issue Date
2015-10-30
Citation
Scientific Reports, 5
Type
Article
Article Type
Article
ISSN
2045-2322
Abstract
Mitochondria are important in many essential cellular functions, including energy production, calcium homeostasis, and apoptosis. The organelles are scattered throughout the cytoplasm, but their distribution can be altered in response to local energy demands, such as cell division and neuronal maturation. Mitochondrial distribution is closely associated with mitochondrial fission, and blocking the fission-promoting protein dynamin-related protein 1 (Drp1) activity often results in mitochondrial elongation and clustering. In this study, we observed that mitochondria were preferentially localized at the leading process of migratory adult neural stem cells (aNSCs), whereas neuronal differentiating cells transiently exhibited perinuclear condensation of mitochondria. Inhibiting Drp1 activity altered the typical migratory cell morphology into round shapes while the polarized mitochondrial distribution was maintained. With these changes, aNSCs failed to migrate, and neuronal differentiation was prevented. Because Drp1 blocking also impaired the mitochondrial membrane potential, we tested whether supplementing with L-carnitine, a compound that restores mitochondrial membrane potential and ATP synthesis, could revert the defects induced by Drp1 inhibition. Interestingly, L-carnitine fully restored the aNSC defects, including cell shrinkage, migration, and impaired neuronal differentiation. These results suggest that Drp1 is required for functionally active mitochondria, and supplementing with ATP can restore the defects induced by Drp1 suppression.
URI
http://hdl.handle.net/20.500.11750/2829
DOI
10.1038/srep15962
Publisher
Nature Publishing Group
Files:
There are no files associated with this item.
Collection:
Brain and Cognitive SciencesETC1. Journal Articles


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