期刊
CURRENT BIOLOGY
卷 23, 期 18, 页码 1818-1824出版社
CELL PRESS
DOI: 10.1016/j.cub.2013.07.053
关键词
-
资金
- Public Health Service grant [GM039066]
- National Institutes of Health National Research Service Award fellowship [F32GM097999]
Active segregation of essential organelles is required for successful cell division. The essential budding yeast myosin V Myo2 actively segregates most organelles along polarized actin cables [1, 2]. The mechanism of mitochondrial segregation remains controversial, with movement driven by actin polymerization [3-5], movement driven by association with transported cortical endoplasmic reticulum (ER) [6, 7], and direct transport by Myo2 [8-11] proposed as models. Two nonessential proteins, Mmr1 and the Rab GTPase Ypt11, bind Myo2 and have been implicated in mitochondrial inheritance, although their specific roles are also contended [7-9, 11]. We generated myo2(sens) mutations that exhibit no overt phenotype but render MMR1 essential and have compromised Ypt11 binding. We then isolated myo2(sens) mmr1(ts) conditional mutants and determined that they have a specific and severe defect in active mitochondrial inheritance, revealing mitochondrial transport by Myo2 as an essential function. ypt11 Delta mmr1(ts) cells also have conditional defects in growth and active transport of mitochondria into the bud, both of which are suppressed by artificially forcing mitochondria! inheritance. At the restrictive temperature, cells defective in mitochondrial inheritance give rise to dead buds that go through cytokinesis normally, showing no evidence of a proposed cell-cycle mitochondrial inheritance checkpoint [12]. Thus, active mitochondrial inheritance is an essential process and a function of Myo2 that requires either Mmr1 or Ypt11.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据