[細胞生物學] 植物在細胞分裂時會利用Katanin來維持細胞微管的長度以促進胞質分裂和細胞板合成。20191127 Current Biology

A Novel Katanin-Tethering Machinery Accelerates Cytokinesis

Takema Sasaki, Motosuke Tsutsumi, Kohei Otomo, Takashi Murata, Noriyoshi Yagi, Masayoshi Nakamura, Tomomi Nemoto, Mitsuyasu Hasebe, and Yoshihisa Oda

Summary

Cytokinesis is fundamental for cell proliferation. In plants, a bipolar short-microtubule array forms the phragmoplast, which mediates vesicle transport to the midzone and guides the formation of cell walls that separate the mother cell into two daughter cells. The phragmoplast centrifugally expands toward the cell cortex to guide cell-plate formation at the cortical division site. Several proteins in the phragmoplast midzone facilitate the anti-parallel bundling of microtubules and vesicle accumulation. However, the mechanisms by which short microtubules are maintained during phragmoplast development, in particular, the behavior of microtubules at the distal zone of phragmoplasts, are poorly understood. Here, we show that a plant-specific protein, CORTICAL MICROTUBULE DISORDERING 4 (CORD4), tethers the conserved microtubulesevering protein katanin to facilitate formation of the short-microtubule array in phragmoplasts. CORD4 was specifically expressed during mitosis and localized to preprophase bands and phragmoplast microtubules. Custom-made two-photon spinning disk confocal microscopy revealed that CORD4 rapidly localized to microtubules in the distal phragmoplast zone during phragmoplast assembly at late anaphase and persisted throughout phragmoplast expansion. Loss of CORD4 caused abnormally long and oblique phragmoplast microtubules and slow expansion of phragmoplasts. The p60 katanin subunit, KTN1, localized to the distal phragmoplast zone in a CORD4-dependent manner. These results suggest that CORD4 tethers KTN1 at phragmoplasts to modulate microtubule length, thereby accelerating phragmoplast growth. This reveals the presence of a distinct machinery to accelerate cytokinesis by regulating the action of katanin.

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拴住Katanin而促進胞質分裂的新機制

總結

胞質分裂在植物的細胞增生中，扮演很關鍵的角色。成膜體是由兩兩成對的雙極性的短細胞微管陣列所組成，引導了微泡到細胞的中央區域來進行細胞壁的形成，最終將母細胞分裂成兩個子細胞。成模體會以同心圓的方式由細胞中心向外擴張至細胞表面，來引導細胞壁的生成。許多在成膜體中央區域的蛋白質會促進反平行的細胞微管形成以及微泡的累積。然而，這些短的微管如何在成膜體發展的過程中維持，特別是在離成膜體較遠的一端的行為，我們非常的不了解。在此，我們展示了一個植物特有的蛋白質，CORD4，可以拴住會將細胞微管裁切的蛋白質-Katanin，來促進在成模體中短微管陣列的形成。CORD4只在有絲分裂時會專一的表現，並且會座落在早前期帶以及成膜體微管上。利用客製化的雙光子轉盤共軛焦顯微鏡的研究顯示，CORD4在細胞分裂後期，會快速的坐落在細胞微管離成膜體較遠的一端並且一直維持到成膜體擴張的階段。當缺少CORD4的時候，會造成異常長以及傾斜的成模體微管，並且出現擴張的成膜體。p60 katanin的一員，KTN1，會以依靠CORD4的方式來座落在離成膜體較遠的一端。這些結果顯示，CORD4會在成膜體的位置抓住KTN1來調節細胞微管的長度，藉此來促進成膜體的成長。這表示了有利用調節katanin的功能來促進胞質分裂的一個特殊機制的存在。

原文出處： https://www.cell.com/current-biology/fulltext/S0960-9822(19)31240-0?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0960982219312400%3Fshowall%3Dtrue