The Rap2c GTPase facilitates B cell receptor-induced reorientation of the microtubule-organizing center.

Q2 Biochemistry, Genetics and Molecular Biology
Small GTPases Pub Date : 2020-11-01 Epub Date: 2018-03-08 DOI:10.1080/21541248.2018.1441626
Jia C Wang, Jeff Y-J Lee, May Dang-Lawson, Caitlin Pritchard, Michael R Gold
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引用次数: 7

Abstract

When B lymphocytes encounter antigen-bearing surfaces, B-cell receptor (BCR) signaling initiates remodeling of the F-actin network and reorientation of the microtubule-organizing center (MTOC) towards the antigen contact site. We have previously shown that the Rap1 GTPase, an evolutionarily conserved regulator of cell polarity, is essential for these processes and that Rap1-regulated actin remodeling is required for MTOC polarization. The role of Rap2 proteins in establishing cell polarity is not well understood. We now show that depleting Rap2c, the only Rap2 isoform expressed in the A20 B-cell line, impairs BCR-induced MTOC reorientation as well as the actin remodeling that supports MTOC polarization. Thus Rap1 and Rap2 proteins may have similar but non-redundant functions in coupling the BCR to MTOC polarization.

Rap2c GTPase促进B细胞受体诱导的微管组织中心的重定向。
当B淋巴细胞遇到携带抗原的表面时,B细胞受体(BCR)信号传导启动f -肌动蛋白网络的重塑和微管组织中心(MTOC)向抗原接触部位的重新定向。我们之前已经证明,Rap1 GTPase是一种进化保守的细胞极性调节剂,对这些过程至关重要,Rap1调节的肌动蛋白重塑是MTOC极化所必需的。Rap2蛋白在建立细胞极性中的作用尚不清楚。我们现在发现,在A20 b细胞系中唯一表达的Rap2亚型Rap2c的缺失,会损害bcr诱导的MTOC重定向以及支持MTOC极化的肌动蛋白重塑。因此,Rap1和Rap2蛋白在BCR与MTOC极化耦合方面可能具有相似但非冗余的功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Small GTPases
Small GTPases Biochemistry, Genetics and Molecular Biology-Biochemistry
CiteScore
6.10
自引率
0.00%
发文量
6
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