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内质网应激时肌醇需求的增加是通过激活 mTORC1 信号来实现的。

Golgi enlargement in Arf-depleted yeast cells is due to altered dynamics of cisternal maturation.

机构信息

Advanced Centre for Treatment Research & Education in Cancer (ACTREC), Tata Memorial Centre, Kharghar, Navi Mumbai, 410210 MH, India.

出版信息

J Cell Sci. 2014 Jan 1;127(Pt 1):250-7. doi: 10.1242/jcs.140996. Epub 2013 Nov 4.

Abstract

Regulation of the size and abundance of membrane compartments is a fundamental cellular activity. In Saccharomyces cerevisiae, disruption of the ADP-ribosylation factor 1 (ARF1) gene yields larger and fewer Golgi cisternae by partially depleting the Arf GTPase. We observed a similar phenotype with a thermosensitive mutation in Nmt1, which myristoylates and activates Arf. Therefore, partial depletion of Arf is a convenient tool for dissecting mechanisms that regulate Golgi structure. We found that in arf1Δ cells, late Golgi structure is particularly abnormal, with the number of late Golgi cisternae being severely reduced. This effect can be explained by selective changes in cisternal maturation kinetics. The arf1Δ mutation causes early Golgi cisternae to mature more slowly and less frequently, but does not alter the maturation of late Golgi cisternae. These changes quantitatively explain why late Golgi cisternae are fewer in number and correspondingly larger. With a stacked Golgi, similar changes in maturation kinetics could be used by the cell to modulate the number of cisternae per stack. Thus, the rates of processes that transform a maturing compartment can determine compartmental size and copy number.

摘要

膜隔室的大小和丰度的调节是一种基本的细胞活动。在酿酒酵母中,通过部分耗尽 Arf GTPase,破坏 ADP-ribosylation 因子 1(ARF1)基因会产生更大和更少的高尔基体潴泡。我们在 Nmt1 的热敏感突变体中观察到类似的表型,Nmt1 酰化并激活 Arf。因此,Arf 的部分耗尽是用于剖析调节高尔基体结构的机制的便捷工具。我们发现,在 arf1Δ 细胞中,晚期高尔基体结构特别异常,晚期高尔基体潴泡的数量严重减少。这种效应可以通过顺式膜成熟动力学的选择性变化来解释。arf1Δ 突变导致早期高尔基体潴泡成熟更慢且更不频繁,但不会改变晚期高尔基体潴泡的成熟。这些变化定量地解释了为什么晚期高尔基体潴泡数量较少且相应较大。在堆叠的高尔基体中,类似的成熟动力学变化可被细胞用来调节每个堆叠中的潴泡数量。因此,将成熟隔室转化的过程的速率可以决定隔室的大小和拷贝数。

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