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pubmed-article:15201867pubmed:abstractTextClass V myosins play a pivotal role in organelle distribution. In the budding yeast, Myo2p, a class V myosin, is essential for mitochondrial distribution. We identified MMR1 as a high-dose suppressor of the myo2 mitochondrial defect and that Mmr1p resides restrictively on the bud-localizing mitochondria and forms a complex with Myo2p tail. Mmr1p loss delayed mitochondrial transfer to buds and completely abolished mitochondrial distribution in the absence of Ypt11p, which promotes mitochondrial distribution by complex formation with Myo2p tail. The myo2-573 mutation, which causes a mitochondrial distribution defect and inactivates the Mmr1p function, reduced association between Myo2p and Mmr1p and depolarized Mmr1p localization on mitochondria. These strongly suggest that Mmr1p is a key mitochondrial component of the link between Myo2p and mitochondria for Myo2p-dependent mitochondrial distribution. Genetical analysis revealed that the Mmr1p-Myo2p pathway is independent of the Ypt11p-Myo2p pathway, suggesting that an essential system for mitochondrial distribution is composed of two independent Myo2p pathways.lld:pubmed
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pubmed-article:15201867pubmed:articleTitleMmr1p is a mitochondrial factor for Myo2p-dependent inheritance of mitochondria in the budding yeast.lld:pubmed
pubmed-article:15201867pubmed:affiliationDepartment of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo, Japan.lld:pubmed
pubmed-article:15201867pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15201867pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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