Mutations that affect vacuole biogenesis inhibit proliferation of the endoplasmic reticulum in Saccharomyces cerevisiae.

Mutations that affect vacuole biogenesis inhibit proliferation of the endoplasmic reticulum in Saccharomyces cerevisiae.
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影响液泡生物发生的突变抑制酿酒酵母内质网的增殖。

DOI:
10.1093/genetics/160.4.1335
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发表时间:
2002
期刊:
影响因子:
3.3
通讯作者:
Wright,RobinL
Wright,RobinL
中科院分区:
生物学2区
文献类型:
--
作者:
Koning,AnnJ;Larson,LynnelleL;Cadera,EmilyJ;Parrish,MarkL;Wright,RobinL

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在酵母中,增加水平的甾醇生物合成酶,3-羟基-3-甲基戊二酰辅酶A(HMG-CoA)还原酶同工酶,Hmg 1 p,诱导组装的核相关的ER膜称为karmament。为了鉴定参与因果报应组装的其他基因,我们筛选了因果报应组装缺陷的温度敏感突变体。两个独立分离的,温度敏感的菌株,也是有缺陷的karmaculum生物进行突变的VPS 16,一个基因参与液泡蛋白分选。在所有13个其他液泡生物合成突变体测试的因果报应生物合成是有缺陷的,虽然因果报应组装缺陷的严重程度取决于特定的突变。14个液泡生物发生突变体衣霉素的超敏反应与明显的karmplant组装缺陷相关,表明karmplant组装缺陷反映了ER结构或功能的改变。与这个假设一致,八个导致分泌缺陷的突变中有七个也影响了业力组装。然而,液泡生物发生突变体能够增殖其ER响应Hmg 2 p,表明突变体没有在ER生物发生过程中的整体缺陷。
In yeast, increased levels of the sterol biosynthetic enzyme, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase isozyme, Hmg1p, induce assembly of nuclear-associated ER membranes called karmellae. To identify additional genes involved in karmellae assembly, we screened temperature-sensitive mutants for karmellae assembly defects. Two independently isolated, temperature-sensitive strains that were also defective for karmellae biogenesis carried mutations inVPS16, a gene involved in vacuolar protein sorting. Karmellae biogenesis was defective in all 13 other vacuole biogenesis mutants tested, although the severity of the karmellae assembly defect varied depending on the particular mutation. The hypersensitivity of 14 vacuole biogenesis mutants to tunicamycin was well correlated with pronounced defects in karmellae assembly, suggesting that the karmellae assembly defect reflected alteration of ER structure or function. Consistent with this hypothesis, seven of eight mutations causing defects in secretion also affected karmellae assembly. However, the vacuole biogenesis mutants were able to proliferate their ER in response to Hmg2p, indicating that the mutants did not have a global defect in the process of ER biogenesis.