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Kinesin-14 motor protein KIFC1 participates in DNA synthesis and chromatin maintenance.
Cell Death & Disease ( IF 8.1 ) Pub Date : 2019-05-24 , DOI: 10.1038/s41419-019-1619-9
Ya-Lan Wei 1 , Wan-Xi Yang 1
Affiliation  

The nuclear localization signal (NLS) in kinesin-14 KIFC1 is associated with nuclear importins and Ran gradient, but detailed mechanism remains unknown. In this study, we found that KIFC1 proteins have specific transport characteristics during cell cycle. In the absence of KIFC1, cell cycle kinetics decrease significantly with a prolonged S phase. After KIFC1 overexpression, the duration of S phase becomes shorten. KIFC1 may transport the recombinant/replicate-related proteins into the nucleus, meanwhile avoiding excessive KIFC1 in the cytoplasm, which results in aberrant microtubule bundling. Interestingly, the deletion of kifc1 in human cells results in a higher ratio of aberrant nuclear membrane, and the degradation of lamin B and lamin A/C. We also found that kifc1 deletion leads to defects in metaphase mitotic spindle assembly, and then results in chromosome structural abnormality. The kifc1-/- cells finally form micronuclei in daughter cells, and results in aneuploidy and chromosome loss in cell cycle. In this study, we demonstrate that kinesin-14 KIFC1 proteins involve in regulating DNA synthesis in S phase, and chromatin maintenance in mitosis, and maintain cell growth in a nuclear transport-independent way.

中文翻译:

Kinesin-14运动蛋白KIFC1参与DNA合成和染色质维持。

驱动蛋白14 KIFC1中的核定位信号(NLS)与核输入蛋白和Ran梯度有关,但详细的机制仍然未知。在这项研究中,我们发现KIFC1蛋白在细胞周期中具有特定的转运特性。在没有KIFC1的情况下,随着S期的延长,细胞周期动力学会显着降低。KIFC1过表达后,S期的持续时间变短。KIFC1可能将重组/复制相关蛋白转运到细胞核中,同时避免了细胞质中过量的KIFC1,从而导致微管束异常束缚。有趣的是,人细胞中kifc1的缺失导致更高比例的异常核膜,以及层粘连蛋白B和层粘连蛋白A / C的降解。我们还发现kifc1缺失会导致中期有丝分裂纺锤体装配中的缺陷,然后导致染色体结构异常。kifc1-/-细胞最终在子细胞中形成微核,并导致细胞周期中的非整倍性和染色体丢失。在这项研究中,我们证明驱动蛋白14 KIFC1蛋白参与调节S期的DNA合成以及有丝分裂中的染色质维持,并以独立于核转运的方式维持细胞生长。
更新日期:2019-05-24
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