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伴侣蛋白介导了从依赖于驱动蛋白-13 的极向运输到后期 B 纺锤体伸长的转换。

Patronin mediates a switch from kinesin-13-dependent poleward flux to anaphase B spindle elongation.

机构信息

Department of Molecular and Cell Biology, University of California, Davis, Davis, CA 95616.

出版信息

J Cell Biol. 2013 Oct 14;203(1):35-46. doi: 10.1083/jcb.201306001. Epub 2013 Oct 7.

Abstract

Anaphase B spindle elongation contributes to chromosome segregation during Drosophila melanogaster embryo mitosis. We propose that this process is driven by a kinesin-5-generated interpolar microtubule (MT; ipMT) sliding filament mechanism that engages when poleward flux is turned off. In this paper, we present evidence that anaphase B is induced by the minus end-stabilizing protein patronin, which antagonizes the kinesin-13 depolymerase KLP10A at spindle poles, thereby switching off the depolymerization of the minus ends of outwardly sliding ipMTs to suppress flux. Although intact cortices, kinetochore MTs, and midzone augmentation are dispensable, this patronin-based change in ipMT minus-end dynamics is sufficient to induce the elongation of spindles capable of separating chromosomes.

摘要

有丝分裂后期 B 期纺锤体的伸长有助于黑腹果蝇胚胎有丝分裂过程中的染色体分离。我们提出,这个过程是由驱动蛋白-5 产生的极间微管(ipMT)滑动丝机制驱动的,当向极运输关闭时,该机制就会启动。在本文中,我们提供的证据表明,有丝分裂后期 B 期是由微管末端稳定蛋白 patronin 诱导的,它在纺锤体两极拮抗驱动蛋白-13 解聚酶 KLP10A,从而停止向外滑动的 ipMT 末端的解聚,以抑制向极运输。尽管完整的皮质、动粒微管和中体扩增是可有可无的,但这种基于 patronin 的 ipMT 末端动力学变化足以诱导能够分离染色体的纺锤体的伸长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/3798244/deba43a34df6/JCB_201306001R_Fig1.jpg

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