Polo kinase phosphorylates Miro to control ER-mitochondria contact sites and mitochondrial Ca2+ homeostasis in neural stem cell development

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dc.contributor.authorSeongsoo Lee-
dc.contributor.authorKyu-Sun Lee-
dc.contributor.authorS Huh-
dc.contributor.authorS Liu-
dc.contributor.authorD Y Lee-
dc.contributor.authorSeung Hyun Hong-
dc.contributor.authorKweon Yu-
dc.contributor.authorB Lu-
dc.date.accessioned2017-04-19T10:20:17Z-
dc.date.available2017-04-19T10:20:17Z-
dc.date.issued2016-
dc.identifier.issn1534-5807-
dc.identifier.uri10.1016/j.devcel.2016.03.023ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13228-
dc.description.abstractMitochondria play central roles in buffering intracellular Ca2+ transients. While basal mitochondrial Ca2+ (Ca2+ mito) is needed to maintain organellar physiology, Ca2+ mito overload can lead to cell death. How Ca2+ mito homeostasis is regulated is not well understood. Here we show that Miro, a known component of the mitochondrial transport machinery, regulates Drosophila neural stem cell (NSC) development through Ca2+ mito homeostasis control, independent of its role in mitochondrial transport. Miro interacts with Ca2+ transporters at the ER-mitochondria contact site (ERMCS). Its inactivation causes Ca2+ mito depletion and metabolic impairment, whereas its overexpression results in Ca2+ mito overload, mitochondrial morphology change, and apoptotic response. Both conditions impaired NSC lineage progression. Ca2+ mito homeostasis is influenced by Polo-mediated phosphorylation of a conserved residue in Miro, which positively regulates Miro localization to, and the integrity of, ERMCS. Our results elucidate a regulatory mechanism underlying Ca2+ mito homeostasis and how its dysregulation may affect NSC metabolism/development and contribute to disease.-
dc.publisherElsevier-Cell Press-
dc.titlePolo kinase phosphorylates Miro to control ER-mitochondria contact sites and mitochondrial Ca2+ homeostasis in neural stem cell development-
dc.title.alternativePolo kinase phosphorylates Miro to control ER-mitochondria contact sites and mitochondrial Ca2+ homeostasis in neural stem cell development-
dc.typeArticle-
dc.citation.titleDevelopmental Cell-
dc.citation.number2-
dc.citation.endPage189-
dc.citation.startPage174-
dc.citation.volume37-
dc.contributor.affiliatedAuthorSeongsoo Lee-
dc.contributor.affiliatedAuthorKyu-Sun Lee-
dc.contributor.affiliatedAuthorSeung Hyun Hong-
dc.contributor.affiliatedAuthorKweon Yu-
dc.contributor.alternativeName이성수-
dc.contributor.alternativeName이규선-
dc.contributor.alternativeName허성운-
dc.contributor.alternativeNameLiu-
dc.contributor.alternativeName이도연-
dc.contributor.alternativeName홍승현-
dc.contributor.alternativeName유권-
dc.contributor.alternativeNameLu-
dc.identifier.bibliographicCitationDevelopmental Cell, vol. 37, no. 2, pp. 174-189-
dc.identifier.doi10.1016/j.devcel.2016.03.023-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > 1. Journal Articles
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