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钙信号传导参与动力蛋白依赖的微管组织。

Calcium signaling is involved in dynein-dependent microtubule organization.

作者信息

Adamíková L'ubica, Straube Anne, Schulz Irene, Steinberg Gero

机构信息

Max-Planck-Institut für terrestrische Mikrobiologie, Karl-von-Frisch-Strabetae, D-35043 Marburg, Germany.

出版信息

Mol Biol Cell. 2004 Apr;15(4):1969-80. doi: 10.1091/mbc.e03-09-0675. Epub 2004 Jan 23.

Abstract

The microtubule cytoskeleton supports cellular morphogenesis and polar growth, but the underlying mechanisms are not understood. In a screen for morphology mutants defective in microtubule organization in the fungus Ustilago maydis, we identified eca1 that encodes a sarcoplasmic/endoplasmic calcium ATPase. Eca1 resides in the endoplasmic reticulum and restores growth of a yeast mutant defective in calcium homeostasis. Deletion of eca1 resulted in elevated cytosolic calcium levels and a severe growth and morphology defect. While F-actin and myosin V distribution is unaffected, Deltaeca1 mutants contain longer and disorganized microtubules that show increased rescue and reduced catastrophe frequencies. Morphology can be restored by inhibition of Ca(2+)/calmodulin-dependent kinases or destabilizing microtubules, indicating that calcium-dependent alterations in dynamic instability are a major cause of the growth defect. Interestingly, dynein mutants show virtually identical changes in microtubule dynamics and dynein-dependent ER motility was drastically decreased in Deltaeca1. This indicates a connection between calcium signaling, dynein, and microtubule organization in morphogenesis of U. maydis.

摘要

微管细胞骨架支持细胞形态发生和极性生长,但其潜在机制尚不清楚。在对玉米黑粉菌中微管组织有缺陷的形态突变体进行的筛选中,我们鉴定出了eca1,它编码一种肌浆网/内质网钙ATP酶。Eca1定位于内质网,并能恢复钙稳态有缺陷的酵母突变体的生长。eca1的缺失导致胞质钙水平升高以及严重的生长和形态缺陷。虽然F-肌动蛋白和肌球蛋白V的分布未受影响,但Deltaeca1突变体含有更长且无序的微管,这些微管表现出更高的拯救频率和更低的灾变频率。通过抑制Ca(2+)/钙调蛋白依赖性激酶或使微管不稳定可以恢复形态,这表明动态不稳定性中钙依赖性改变是生长缺陷的主要原因。有趣的是,动力蛋白突变体在微管动力学上表现出几乎相同的变化,并且在Deltaeca1中动力蛋白依赖性内质网运动显著降低。这表明在玉米黑粉菌的形态发生中钙信号传导、动力蛋白和微管组织之间存在联系。

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本文引用的文献

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