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丝状真菌构巢曲霉中的一个 septin 诱导出芽酵母酿酒酵母中的非典型假菌丝。

A septin from the filamentous fungus A. nidulans induces atypical pseudohyphae in the budding yeast S. cerevisiae.

机构信息

Department of Plant Biology, University of Georgia, Athens, Georgia, United States of America.

出版信息

PLoS One. 2010 Mar 25;5(3):e9858. doi: 10.1371/journal.pone.0009858.

Abstract

BACKGROUND

Septins, novel cytoskeletal proteins, form rings at the bases of emerging round buds in yeasts and at the bases of emerging elongated hyphal initials in filamentous fungi.

METHODOLOGY/PRINCIPAL FINDINGS: When introduced into the yeast Saccharomyces cerevisiae, the septin AspC from the filamentous fungus Aspergillus nidulans induced highly elongated atypical pseudohyphae and spore-producing structures similar to those of hyphal fungi. AspC induced atypical pseudohyphae when S. cerevisiae pseudohyphal or haploid invasive genes were deleted, but not when the CDC10 septin gene was deleted. AspC also induced atypical pseudohyphae when S. cerevisiae genes encoding Cdc12-interacting proteins Bem4, Cla4, Gic1 and Gic2 were deleted, but not when BNI1, a Cdc12-interacting formin gene, was deleted. AspC localized to bud and pseudohypha necks, while its S. cerevisiae ortholog, Cdc12, localized only to bud necks.

CONCLUSIONS/SIGNIFICANCE: Our results suggest that AspC competes with Cdc12 for incorporation into the yeast septin scaffold and once there alters cell shape by altering interactions with the formin Bni1. That introduction of the A. nidulans septin AspC into S. cerevisiae induces a shift from formation of buds to formation of atypical pseudohyphae suggests that septins play an important role in the morphological plasticity of fungi.

摘要

背景

新型细胞骨架蛋白 septin 在酵母中正在形成的圆形芽基底部和丝状真菌中正在形成的伸长丝状初始细胞的基部形成环。

方法/主要发现:当丝状真菌 Aspergillus nidulans 的 septin AspC 被引入酵母 Saccharomyces cerevisiae 中时,它诱导出高度伸长的非典型假菌丝和类似于丝状真菌的产孢结构。当 S. cerevisiae 假菌丝或单倍体侵袭基因缺失时,AspC 诱导出非典型假菌丝,但当 CDC10 septin 基因缺失时则不会。当 S. cerevisiae 编码与 Cdc12 相互作用的蛋白 Bem4、Cla4、Gic1 和 Gic2 的基因缺失时,AspC 也诱导出非典型假菌丝,但当 Cdc12 相互作用的formin 基因 BNI1 缺失时则不会。AspC 定位于芽和假菌丝颈部,而其 S. cerevisiae 同源物 Cdc12 仅定位于芽颈部。

结论/意义:我们的结果表明,AspC 与 Cdc12 竞争掺入酵母 septin 支架,一旦掺入,就通过改变与formin Bni1 的相互作用来改变细胞形状。将 A. nidulans septin AspC 引入 S. cerevisiae 会导致从芽的形成转变为非典型假菌丝的形成,这表明 septin 在真菌形态可塑性中起着重要作用。

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