通过FEM1B的停止密码子阅读来调节细胞循环的类人特异性调节
Md Noor Akhtar1, Anumeha Singh1, Lekha E Manjunath1
1Department of Biochemistry, Indian Institute of Science, Bengaluru 560012, India.
Journal of cell science
|August 14, 2024
概括
停止密码子读透 (SCR) 调节FEM1B的表达,产生一种不稳定的蛋白质. 这种在人类和猿类中新发现的机制通过控制FEM1B水平,影响细胞循环调节.
科学领域:
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
- 细胞生物学 细胞生物学
背景情况:
- FEM1B 作为 CRL2 E3 泛基因结合酶复合物的关键组成部分,调解蛋白质降解.
- 调节蛋白质水平对于细胞过程至关重要,包括细胞循环.
研究的目的:
- 通过停止编码子读透 (SCR) 调查FEM1B表达的调节.
- 阐明FEM1B SCR的机制和进化起源及其对细胞过程的影响.
主要方法:
- 利用CRISPR基因编辑创建缺乏FEM1B SCR cis调节区域的细胞.
- 分析了改变FEM1B表达对下游标,如SLBP和组织蛋白的影响.
- 进行了进化分析,以确定FEM1B SCR的物种特异性.
主要成果:
- 发现停止密码子读透 (SCR) 产生了一个C端扩展的不稳定的FEM1B异形.
- 在FEM1B 3'UTR中确定了一个81核酸区,该区域对于SCR和扩展产品的降解至关重要.
- 为了取消SCR的CRISPR编辑导致FEM1B增加,SLBP和胰岛素表达减少,细胞周期延迟.
- 发现FEM1B SCR特定于Hominini部落 (包括人类和黑猩猩).
结论:
- FEM1B的表达是由最近进化的停止密码子读透 (SCR) 机制调节的.
- 这种SCR过程导致扩展FEM1B异形的降解,从而减轻细胞周期的负调节.
- 这些发现突出了影响灵长类动物细胞周期进展的新型基因表达控制层.
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