在花粉中调节基因表达的对抗性表观遗传机制通过单核多组学揭示
Colette L Picard1,2, Lucia Ichino3,1,2, Tyler J Buckley3,1
1Department of Molecular, Cell and Developmental Biology, University of California Los Angeles, Los Angeles, CA 90095, USA.
bioRxiv : the preprint server for biology
|November 24, 2025
概括
甲基结合域蛋白MBD5/6抑制了花粉植物核中的基因表达. 丢失MBD7通过促进脱甲基化来挽救这些缺陷,揭示了一个新的调节途径.
科学领域:
- 植物分子生物学 植物分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 基因调节 基因调节
背景情况:
- 阿拉比多普西斯MBD5,MBD6和MBD7是CG特有的甲基读取器.
- MBD5和MBD6 (MBD5/6) 抑制花粉植物核 (VN) 中的甲基化位点.
- MBD7防止了转基因沉默,可能是通过DNA脱甲基化.
研究的目的:
- 研究VN转录中的MBD5/6,MBD7和DNA甲基化之间的相互作用.
- 确定MBD7在调节MBD5/6-绑定位点中的作用.
- 阐明VN中转录控制的机制.
主要方法:
- 在单个花粉核中同时对DNA甲基化和转录进行分析.
- 对突变系的分析 (MBD7,MBD5/6的损失).
- 宫外招募MBD7复合体到MBD5/6的目标.
主要成果:
- 丢失MBD7可挽救MBD5/6-结合的局部的子集的转录缺陷.
- 在VN中经过脱甲基化的MBD5/6-结合位点在mbd5/6突变体中失去进一步的甲基化,在转录脱压之前.
- 在mbd5/6突变体中,MBD7结合与脱甲基和脱压相关,而MBD7损失则会逆转这种情况.
结论:
- 通过抑制MBD7复合体,MBD5/6可以维持VN沉默,部分是通过抑制MBD7复合体.
- 在VN成熟过程中,MBD7复合物促进了活性去甲基化.
- 在VN中,MBD5/6和MBD7在调节DNA甲基化和转录方面具有相反的作用.
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