通过SETD2修改H3K36me3对于Col11a2和Sema3e转录至关重要,以维持小鼠的牙生成
Jiaxin Niu1,2,3, Jing Fu1,2,3,4, Hao Feng1,2,3
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan 430079, China.
概括
通过SETD2介导的组织素甲基化 (H3K36me3) 对牙形成至关重要. 这一过程涉及调节特定的基因和AKT1信号,这对牙细胞分化和牙生成至关重要.
科学领域:
- 生物化学 生物化学
- 发展生物学 发展生物学
- 遗传学 遗传学 是一个
背景情况:
- 牙的形成 (牙生成) 取决于牙细胞.
- 希斯甲基化会影响牙细胞的分化.
- 李素36甲基化 (H3K36me3) 在牙发生过程中,基因组3在牙发生过程中的具体作用尚不清楚.
研究的目的:
- 研究SETD2的功能,一个H3K36甲基转移酶,在口腔细胞分化和牙生成.
- 阐明SETD2调节这些过程的分子机制.
主要方法:
- 在体外敲除细胞模型中的试验.
- 使用条件淘汰赛小鼠模型的体内研究.
- 综合RNA测序和CUT&Tag测序分析.
- 基因表达分析和西式涂抹.
主要成果:
- 在口腔细胞中,SETD2的表达很高,对牙生成至关重要.
- 缺少SETD2会影响牙细胞的分化和牙的形成.
- SETD2 调节 H3K36me3 的占用率和 Col11a2 和 Sema3e 的转录.
- 通过AKT1信号传递,COL11A2和SEMA3E促进了口腔细胞分化.
- AKT1激活部分挽救了Setd2缺陷引起的缺陷.
结论:
- 由SETD2催化的H3K36me3对于牙生成至关重要.
- 通过控制Col11a2和Sema3e的表达,SETD2调节牙生成,这会影响AKT1的信号传递.
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