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gmfA 的缺失可诱导变形虫中的角膜细胞样迁移。

Deletion of gmfA induces keratocyte-like migration in Dictyostelium.

机构信息

Graduate School of Sciences and Technology for Innovation, Yamaguchi University, Japan.

Graduate School of Life and Environmental Sciences, University of Tsukuba, Japan.

出版信息

FEBS Open Bio. 2022 Jan;12(1):306-319. doi: 10.1002/2211-5463.13339. Epub 2021 Dec 12.

DOI:10.1002/2211-5463.13339
PMID:34855306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8727941/
Abstract

Glia maturation factor (GMF) has been established as an inactivating factor of the actin-related protein 2/3 (Arp2/3) complex, which regulates actin assembly. Regulation of actin assembly and reorganization is crucial for various cellular events, such as cell migration, cell division, and development. Here, to examine the roles of ADF-H domain-containing protein (also known as glia maturation factor; GmfA), the product of a single GMF homologous gene in Dictyostelium, gmfA-null cells were generated. They had moderate defects in cell growth and cytokinesis. Interestingly, they showed a keratocyte-like fan shape with a broader pseudopod, where Arp3 accumulated at higher levels than in wild-type cells. They migrated with higher persistence, but their velocities were comparable to those of wild-type cells. The polar pseudopods during cell division were also broader than those in wild-type cells. However, GmfA did not localize at the pseudopods in migrating cells or the polar pseudopods in dividing cells. Adhesions of mutant cells to the substratum were much stronger than that of wild-type cells. Although the mutant cells showed chemotaxis comparable to that of wild-type cells, they formed disconnected streams during the aggregation stage; however, they finally formed normal fruiting bodies. These results suggest that GmfA plays a crucial role in cell migration.

摘要

胶质成熟因子 (GMF) 已被确立为肌动蛋白相关蛋白 2/3 (Arp2/3) 复合物的失活因子,该复合物调节肌动蛋白组装。肌动蛋白组装和重排的调节对于各种细胞事件至关重要,例如细胞迁移、细胞分裂和发育。在这里,为了研究 ADF-H 结构域蛋白(也称为胶质成熟因子;GmfA)的作用,该蛋白是 Dictyostelium 中单个 GMF 同源基因的产物,生成了 gmfA 缺失细胞。它们在细胞生长和胞质分裂方面存在中度缺陷。有趣的是,它们表现出类似于角膜细胞的扇形,具有更宽的伪足,其中 Arp3 积累水平高于野生型细胞。它们以更高的持久性迁移,但它们的速度与野生型细胞相当。细胞分裂过程中的极性伪足也比野生型细胞宽。然而,GmfA 并不定位在迁移细胞中的伪足或分裂细胞中的极性伪足中。突变细胞与基底的粘附比野生型细胞强得多。尽管突变细胞表现出与野生型细胞相当的趋化性,但它们在聚集阶段形成不连续的流;然而,它们最终形成了正常的子实体。这些结果表明 GmfA 在细胞迁移中发挥着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/ef633350e9b2/FEB4-12-306-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/4bf891736cf5/FEB4-12-306-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/507d2fe45717/FEB4-12-306-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/37a3415012c8/FEB4-12-306-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/875b278cb625/FEB4-12-306-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/ef633350e9b2/FEB4-12-306-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/4bf891736cf5/FEB4-12-306-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/507d2fe45717/FEB4-12-306-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/37a3415012c8/FEB4-12-306-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/875b278cb625/FEB4-12-306-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ac/8727941/ef633350e9b2/FEB4-12-306-g002.jpg

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