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减数分裂纺锤体极体上的Hrs1p/Mcp6p蛋白为振荡性核运动组织星体微管阵列。

Hrs1p/Mcp6p on the meiotic SPB organizes astral microtubule arrays for oscillatory nuclear movement.

作者信息

Tanaka Kayoko, Kohda Toshiki, Yamashita Akira, Nonaka Nobuhiro, Yamamoto Masayuki

机构信息

Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Hongo, Tokyo 113-0033, Japan.

出版信息

Curr Biol. 2005 Aug 23;15(16):1479-86. doi: 10.1016/j.cub.2005.07.058.

Abstract

Microtubules and the motor protein dynein play pivotal roles in the movement and positioning of the nucleus and cytoplasmic organelles in a cell. In fission yeast, oscillatory movement of the nucleus termed horsetail nuclear movement (HNM) has been observed during meiotic prophase. HNM is led by an astral microtubule array emanating from the spindle pole body (SPB), a centrosome-equivalent organelle in yeasts, aided by the dynein-dynactin complex, and is proposed to facilitate the alignment of homologous chromosomes necessary for efficient meiotic recombination. Here we show that a meiosis-specific SPB component Hrs1p (also known as Mcp6p) is a key molecule to remodel microtubules into the horsetail-astral array (HAA). Deletion of Hrs1p impaired HAA formation, leading to compromised HNM. Ectopic expression of Hrs1p during the mitotic cell cycle resulted in the formation of a HAA-like astral microtubule array, which drove an oscillatory nuclear movement in interphase cells. Hrs1p interacted with components of the gamma-tubulin ring complex (gamma-TuRC) as well as with a meiotic SPB component. We propose that Hrs1p facilitates formation of the HAA, responsible for the vigorous HNM, by stabilizing connection between the SPB and minus ends of microtubules.

摘要

微管和动力蛋白驱动蛋白在细胞内核和细胞质细胞器的移动及定位过程中发挥着关键作用。在裂殖酵母中,减数分裂前期会观察到细胞核的振荡运动,即马尾状核运动(HNM)。HNM由源自纺锤体极体(SPB,酵母中与中心体等效的细胞器)的星体微管阵列引导,并在驱动蛋白-动力蛋白激活蛋白复合体的辅助下进行,其作用是促进高效减数分裂重组所需的同源染色体配对。在此,我们表明减数分裂特异性SPB组分Hrs1p(也称为Mcp6p)是将微管重塑为马尾状星体阵列(HAA)的关键分子。缺失Hrs1p会损害HAA的形成,导致HNM受损。在有丝分裂细胞周期中异位表达Hrs1p会导致形成类似HAA的星体微管阵列,从而在间期细胞中驱动振荡核运动。Hrs1p与γ-微管蛋白环复合体(γ-TuRC)的组分以及减数分裂SPB组分相互作用。我们认为,Hrs1p通过稳定SPB与微管负端之间的连接来促进HAA的形成,而HAA负责剧烈的HNM。

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