Mitochondrial inheritance is delayed in Saccharomyces cerevisiae cells lacking the serine/threonine phosphatase PTC1
Mitochondrial inheritance is delayed in Saccharomyces cerevisiae cells lacking the serine/threonine phosphatase PTC1
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DOI：
10.1091/mbc.9.4.917
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发表时间：
1998-04-01
影响因子：
3.3
通讯作者：
Shaw, JM
中科院分区：
文献类型：
--
作者：
Roeder, AD;Hermann, GJ;Shaw, JM
在野生型酵母中，线粒体遗传发生在细胞周期的早期，伴随着芽的出现。缺乏PTC1基因的细胞最初产生的芽没有线粒体隔室；然而，这些芽随后接收来自母细胞的部分线粒体网络。因此，PTC1的缺失导致线粒体运输的延迟，但不是完全阻断。PTC1在高渗透压甘油反应（HOG）途径中编码丝氨酸/苏氨酸磷酸酶。ptc1突变体的线粒体遗传延迟不能归因于细胞内甘油浓度的变化或肌动蛋白细胞骨架组织的缺陷。此外，ptc1 δ和HOG途径激酶突变的上位实验表明，ptc1不通过HOG途径控制线粒体遗传的时间。相反，PTC1可能直接或通过不同的信号通路影响细胞中的线粒体运输机制。这些研究表明，野生型细胞中线粒体运输的时间是遗传控制的，并提供了线粒体遗传不依赖于线粒体网络和初芽位点之间的物理联系的新证据。
In wild-type yeast mitochondrial inheritance occurs early in the cell cycle concomitant with bud emergence. Cells lacking the PTC1 gene initially produce buds without a mitochondrial compartment; however, these buds later receive part of the mitochondrial network from the mother cell. Thus, the loss of PTC1 causes a delay, but not a complete block, in mitochondrial transport. PTC1 encodes a serine/threonine phosphatase in the high-osmolarity glycerol response (HOG) pathway. The mitochondrial inheritance delay in the ptc1 mutant is not attributable to changes in intracellular glycerol concentrations or defects in the organization of the actin cytoskeleton. Moreover, epistasis experiments with ptc1 Delta and mutations in HOG pathway kinases reveal that PTC1 is not acting through the HOG pathway to control the timing of mitochondrial inheritance. Instead, PTC1 may be acting either directly or through a different signaling pathway to affect the mitochondrial transport machinery in the cell. These studies indicate that the timing of mitochondrial transport in wild-type cells is genetically controlled and provide new evidence that mitochondrial inheritance does not depend on a physical link between the mitochondrial network and the incipient bud site.