Roeder A D, Hermann G J, Keegan B R, Thatcher S A, Shaw J M
Department of Biology, University of Utah, Salt Lake City, Utah 84112, USA.
Mol Biol Cell. 1998 Apr;9(4):917-30. doi: 10.1091/mbc.9.4.917.
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 ptc1delta 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.
在野生型酵母中,线粒体遗传发生在细胞周期早期,与芽的出现同时发生。缺乏PTC1基因的细胞最初产生的芽没有线粒体区室;然而,这些芽随后从母细胞接收部分线粒体网络。因此,PTC1的缺失导致线粒体运输延迟,但并非完全阻断。PTC1在高渗甘油应答(HOG)途径中编码一种丝氨酸/苏氨酸磷酸酶。ptc1突变体中线粒体遗传延迟并非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,对ptc1delta和HOG途径激酶突变进行的上位性实验表明,PTC1并非通过HOG途径来控制线粒体遗传的时间。相反,PTC1可能直接起作用,或通过不同的信号通路来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受基因控制的,并提供了新的证据,证明线粒体遗传不依赖于线粒体网络与初始芽位点之间的物理连接。