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KASH蛋白Kms2协调纺锤极体的有丝分裂重塑。

The KASH protein Kms2 coordinates mitotic remodeling of the spindle pole body.

作者信息

Wälde Sarah, King Megan C

机构信息

Department of Cell Biology, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA.

Department of Cell Biology, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA

出版信息

J Cell Sci. 2014 Aug 15;127(Pt 16):3625-40. doi: 10.1242/jcs.154997. Epub 2014 Jun 24.

Abstract

Defects in the biogenesis of the spindle pole body (SPB), the yeast centrosome equivalent, can lead to monopolar spindles and mitotic catastrophe. The KASH domain protein Kms2 and the SUN domain protein Sad1 colocalize within the nuclear envelope at the site of SPB attachment during interphase and at the spindle poles during mitosis in Schizosaccharomyces pombe. We show that Kms2 interacts with the essential SPB components Cut12 and Pcp1 and the Polo kinase Plo1. Depletion of Kms2 delays mitotic entry and leads to defects in the insertion of the SPB into the nuclear envelope, disrupting stable bipolar spindle formation. These effects are mediated in part by a delay in the recruitment of Plo1 to the SPB at mitotic entry. Plo1 activity supports mitotic SPB remodeling by driving a burst of incorporation of Cut12 and Pcp1. Thus, a fission yeast SUN-KASH complex plays an important role in supporting the remodeling of the SPB at mitotic entry.

摘要

纺锤极体(SPB)相当于酵母中的中心体,其生物发生缺陷可导致单极纺锤体和有丝分裂灾难。在裂殖酵母中,KASH结构域蛋白Kms2和SUN结构域蛋白Sad1在间期于核膜内SPB附着位点共定位,在有丝分裂期于纺锤极共定位。我们发现,Kms2与必需的SPB组分Cut12和Pcp1以及Polo激酶Plo1相互作用。Kms2的缺失会延迟有丝分裂进入,并导致SPB插入核膜出现缺陷,破坏稳定的双极纺锤体形成。这些效应部分是由有丝分裂进入时Plo1募集到SPB的延迟介导的。Plo1活性通过驱动Cut12和Pcp1的一阵掺入来支持有丝分裂SPB重塑。因此,裂殖酵母的SUN-KASH复合体在支持有丝分裂进入时SPB的重塑中起重要作用。

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