纺锤体位置检查点激酶Kin4对细胞器运输的时空调控

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Journal of cell science Pub Date : 2024-11-01 Epub Date: 2024-11-13 DOI:10.1242/jcs.261948
Lakhan Ekal, Abdulaziz M S Alqahtani, Kathryn R Ayscough, Ewald H Hettema
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引用次数: 0

摘要

酿酒酵母(Saccharomyces cerevisiae)的非对称细胞分裂涉及 V 类肌球蛋白依赖性细胞器沿极化肌动蛋白细胞骨架向新芽的运输。Vac17 是液泡/溶酶体特异性肌球蛋白受体。它的及时分解会终止运输,并使液泡在芽中正确定位。Vac17 的分解受芽集中的 p21 激活激酶 Cla4 和 E3 泛素连接酶 Dma1 控制。我们发现,纺锤体位置检查点激酶Kin4及其同系物Frk1能阻止Cla4和Dma1过早分解Vac17,从而有助于成功的液泡运输。此外,Kin4 和 Cla4 还有助于调节过氧物酶体的转运。我们的结论是,Kin4与Cla4/Dma1途径起拮抗作用,协调细胞器转运的时空调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Spatiotemporal regulation of organelle transport by spindle position checkpoint kinase Kin4.

Asymmetric cell division in Saccharomyces cerevisiae involves class V myosin-dependent transport of organelles along the polarised actin cytoskeleton to the emerging bud. Vac17 is the vacuole/lysosome-specific myosin receptor. Its timely breakdown terminates transport and results in the proper positioning of vacuoles in the bud. Vac17 breakdown is controlled by the bud-concentrated p21-activated kinase Cla4, and the E3-ubiquitin ligase Dma1. We found that the spindle position checkpoint kinase Kin4 and, to a lesser extent, its paralog Frk1 contribute to successful vacuole transport by preventing the premature breakdown of Vac17 by Cla4 and Dma1. Furthermore, Kin4 and Cla4 contribute to the regulation of peroxisome transport. We conclude that Kin4 antagonises the Cla4/Dma1 pathway to coordinate spatiotemporal regulation of organelle transport.

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来源期刊
Journal of cell science
Journal of cell science 生物-细胞生物学
CiteScore
7.30
自引率
2.50%
发文量
393
审稿时长
1.4 months
期刊介绍: Journal of Cell Science publishes cutting-edge science, encompassing all aspects of cell biology.
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