Ras小GTP酶在各种细胞信号通路中充当分子开关,包括细胞迁移,扩散,和差异化。三种Rap蛋白存在于网藻中;RapA,拉普,还有RapC.据报道RapA和RapC在控制细胞粘附和迁移方面具有相反的功能。这里,我们调查了RapB的作用,网菌属RasGTPase亚家族的成员,专注于它参与细胞粘附,迁移,和发展过程。这项研究显示RapB,类似于RapA,在调节细胞形态中起着至关重要的作用,附着力,和移民。rapB空细胞,它们是由CRISPR/Cas9基因编辑产生的,显示更改的单元格大小,减少细胞-基质粘附,趋化过程中的迁移速度增加。通过RapB和RapA的表达恢复了这些rapB无效细胞的表型,但不是RapC.与这些结果一致,拉普,类似于RapA,未能挽救rapC无效细胞的表型,扩散形态,细胞粘附增加,趋化过程中迁移速度降低。rapB无效细胞的多细胞发育未受影响。这些结果表明RapB参与控制细胞形态和细胞粘附。重要的是,RapB在趋化过程中似乎在调节迁移速度中起抑制作用,可能通过控制细胞-基质粘附,类似RapA的功能。这些发现有助于理解Ras亚家族蛋白之间的功能关系。
Ras small GTPases act as molecular switches in various cellular signaling pathways, including cell migration, proliferation, and differentiation. Three Rap proteins are present in Dictyostelium; RapA, RapB, and RapC. RapA and RapC have been reported to have opposing functions in the control of cell adhesion and migration. Here, we investigated the role of RapB, a member of the Ras GTPase subfamily in Dictyostelium, focusing on its involvement in cell adhesion, migration, and developmental processes. This study revealed that RapB, similar to RapA, played a crucial role in regulating cell morphology, adhesion, and migration. rapB null cells, which were generated by CRISPR/Cas9 gene editing, displayed altered cell size, reduced cell-substrate adhesion, and increased migration speed during chemotaxis. These phenotypes of rapB null cells were restored by the expression of RapB and RapA, but not RapC. Consistent with these results, RapB, similar to RapA, failed to rescue the phenotypes of rapC null cells, spread morphology, increased cell adhesion, and decreased migration speed during chemotaxis. Multicellular development of rapB null cells remained unaffected. These results suggest that RapB is involved in controlling cell morphology and cell adhesion. Importantly, RapB appears to play an inhibitory role in regulating the migration speed during chemotaxis, possibly by controlling cell-substrate adhesion, resembling the functions of RapA. These findings contribute to the understanding of the functional relationships among Ras subfamily proteins.