高/万格氨酸酸化开关调节其与核心平面细胞的相互作用 极性因子 刺痛和不整形
Ashley C Humphries1, Claudia Molina-Pelayo1, Parijat Sil2
1Dept. of Cell, Developmental, & Regenerative Biology,Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
PLoS genetics
|July 18, 2023
概括
平面细胞极性 (PCP) 涉及Vang/Vangl蛋白质酸化. 这种修改促进了与Prickle (Pk) 的结合,同时抑制了Dishevelled (Dsh/Dvl) 的相互作用,调节了PCP复合体的形成.
科学领域:
- 细胞生物学 细胞生物学
- 发展生物学 发展生物学
- 分子生物学分子生物学
背景情况:
- 表皮组织表现出基极性和平面细胞极性 (PCP).
- 平面细胞极性依赖于保存的Wnt/Frizzled (Fz) 信号通路,包括高 (Vang/Vangl).
研究的目的:
- 调查Vang/Vangl酸化对特定的氨酸残留物如何影响与Dishevelled (Dsh/Dvl) 和Prickle (Pk) 的相互作用.
- 阐明Vang/Vangl酸化在调节平面细胞极性建立中的作用.
主要方法:
- 在Drosophila翅膀和小鼠皮肤中建立PCP的比较分析.
- 生物化学测试以评估Vang/Vangl和核心PCP因子之间的蛋白质-蛋白质相互作用.
主要成果:
- Dishevelled (Dsh/Dvl) 和 Prickle (Pk) 结合到Vang/Vangl上的重叠区域,中心围绕着一个保存的氨酸残留物.
- 化Vang/Vangl在这种氨酸促进Prickle (Pk) 结合,并抑制Dish (Dsh/Dvl) 相互作用.
- 这种酸化起到切换作用,有利于稳定的Vang/Vangl-Pk复合体形成,而不是短暂的Vang/Vangl-Dishevelled相互作用.
结论:
- 旺格/万格氨酸酸化是平面细胞极性的一个关键调节机制.
- 酸化控制了对抗性PCP因子Dsh/Dvl和Pk之间的平衡,影响了复合体的稳定性和PCP途径的进展.
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