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一项全基因组筛选揭示了内吞基因在. 细胞分裂过程中 Pma1p 不对称性中的重要作用。

A Genome-Wide Screen Reveals That Endocytic Genes Are Important for Pma1p Asymmetry during Cell Division in .

机构信息

School of Life Sciences, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 61005, Korea.

Cell Logistics Research Center, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 61005, Korea.

出版信息

Int J Mol Sci. 2022 Feb 21;23(4):2364. doi: 10.3390/ijms23042364.

DOI:10.3390/ijms23042364
PMID:35216480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8874555/
Abstract

An asymmetry in cytosolic pH between mother and daughter cells was reported to underlie cellular aging in the budding yeast ; however, the underlying mechanism remains unknown. Preferential accumulation of Pma1p, which pumps cytoplasmic protons out of cells, at the plasma membrane of mother cells, but not of their newly-formed daughter cells, is believed to be responsible for the pH increase in mother cells by reducing the level of cytoplasmic protons. This, in turn, decreases the acidity of vacuoles, which is well correlated with aging of yeast cells. In this study, to identify genes that regulate the preferential accumulation of Pma1p in mother cells, we performed a genome-wide screen using a collection of single gene deletion yeast strains. A subset of genes involved in the endocytic pathway, such as , , and , was important for Pma1p accumulation. Unexpectedly, however, there was little correlation between deletion of each of these genes and the replicative lifespan of yeast, suggesting that Pma1p accumulation in mother cells is not the key determinant that underlies aging of mother cells.

摘要

细胞内细胞质 pH 在母细胞和子细胞之间的不对称性被报道为酵母出芽过程中细胞衰老的基础;然而,其潜在机制尚不清楚。人们认为,Pma1p(一种将细胞质质子泵出细胞的蛋白)优先积累在母细胞的质膜上,而不是新形成的子细胞的质膜上,这导致了母细胞中细胞质质子水平的降低,从而导致了液泡酸度的降低,这与酵母细胞的衰老密切相关。在这项研究中,为了鉴定调节 Pma1p 在母细胞中优先积累的基因,我们使用一组单基因缺失酵母菌株进行了全基因组筛选。一组参与内吞途径的基因,如、和,对 Pma1p 的积累很重要。然而,出乎意料的是,这些基因中的每一个缺失与酵母的复制寿命之间几乎没有相关性,这表明 Pma1p 在母细胞中的积累并不是导致母细胞衰老的关键决定因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/ef9c317291d6/ijms-23-02364-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/bf118a1fc141/ijms-23-02364-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/835db85e7b7d/ijms-23-02364-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/d4fab010d784/ijms-23-02364-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/f9fc4059d9e0/ijms-23-02364-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/2c5e7907f5af/ijms-23-02364-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/ef9c317291d6/ijms-23-02364-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/bf118a1fc141/ijms-23-02364-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/835db85e7b7d/ijms-23-02364-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/d4fab010d784/ijms-23-02364-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/f9fc4059d9e0/ijms-23-02364-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/2c5e7907f5af/ijms-23-02364-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e20/8874555/ef9c317291d6/ijms-23-02364-g006.jpg

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