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在双向细胞器运输过程中,动力蛋白、动力蛋白激活蛋白和驱动蛋白II与微管的相互作用受到调控。

Dynein, dynactin, and kinesin II's interaction with microtubules is regulated during bidirectional organelle transport.

作者信息

Reese E L, Haimo L T

机构信息

Department of Biology, University of California at Riverside, Riverside, California 92521, USA.

出版信息

J Cell Biol. 2000 Oct 2;151(1):155-66. doi: 10.1083/jcb.151.1.155.

Abstract

The microtubule motors, cytoplasmic dynein and kinesin II, drive pigmented organelles in opposite directions in Xenopus melanophores, but the mechanism by which these or other motors are regulated to control the direction of organelle transport has not been previously elucidated. We find that cytoplasmic dynein, dynactin, and kinesin II remain on pigment granules during aggregation and dispersion in melanophores, indicating that control of direction is not mediated by a cyclic association of motors with these organelles. However, the ability of dynein, dynactin, and kinesin II to bind to microtubules varies as a function of the state of aggregation or dispersion of the pigment in the cells from which these molecules are isolated. Dynein and dynactin bind to microtubules when obtained from cells with aggregated pigment, whereas kinesin II binds to microtubules when obtained from cells with dispersed pigment. Moreover, the microtubule binding activity of these motors/dynactin can be reversed in vitro by the kinases and phosphatase that regulate the direction of pigment granule transport in vivo. These findings suggest that phosphorylation controls the direction of pigment granule transport by altering the ability of dynein, dynactin, and kinesin II to interact with microtubules.

摘要

微管马达蛋白,胞质动力蛋白和驱动蛋白II,在非洲爪蟾黑素细胞中驱动色素细胞器向相反方向移动,但此前尚未阐明这些或其他马达蛋白如何被调控以控制细胞器运输方向的机制。我们发现,在黑素细胞聚集和分散过程中,胞质动力蛋白、动力蛋白激活蛋白和驱动蛋白II始终附着在色素颗粒上,这表明方向控制并非由马达蛋白与这些细胞器的循环结合介导。然而,动力蛋白、动力蛋白激活蛋白和驱动蛋白II与微管结合的能力会随着从分离出这些分子的细胞中色素的聚集或分散状态而变化。当从色素聚集的细胞中获取时,动力蛋白和动力蛋白激活蛋白会与微管结合,而当从色素分散的细胞中获取时,驱动蛋白II会与微管结合。此外,这些马达蛋白/动力蛋白激活蛋白的微管结合活性在体外可被体内调节色素颗粒运输方向的激酶和磷酸酶逆转。这些发现表明,磷酸化通过改变动力蛋白、动力蛋白激活蛋白和驱动蛋白II与微管相互作用的能力来控制色素颗粒运输的方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0900/2189799/36ff35e3ef6a/JCB0006060.f1.jpg

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