Bmi1通过全基因组H3K27me3修改控制听觉感官上皮细胞的增殖
Xiaoling Lu1, Yunzhong Zhang1, Ruofei Dai2
1Department of ENT Institute and Otorhinolaryngology, Eye & ENT Hospital, Shanghai Key Laboratory of Gene Editing and Cell Therapy for Rare Diseases, NHC Key Laboratory of Hearing Medicine Research, Fudan University, Shanghai, 200032, People's Republic of China.
在新生小鼠中,Bmi1蛋白减少会通过改变基因表达和染色质可访问性而导致毛细胞脱落. 抑制Cdkn2c可以挽救细胞增殖,为听力损失提供治疗点.
科学领域:
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 发育生物学 发展生物学
- 听觉神经科学 听觉神经科学
背景情况:
- Bmi1 (多合体抑制复合体1) 通过染色质结构调节基因表达.
- Bmi1的减少导致新生小鼠的耳毛细胞损失.
- 研究Bmi1在听觉上皮质中枯竭的表观遗传机制.
研究的目的:
- 阐明Bmi1枯竭效应背后的表观遗传机制.
- 确定Bmi1在尾细胞中丧失的转录后果.
- 确定听力损失的潜在治疗点.
主要方法:
- Bmi1 淘汰赛小鼠模型.
- H3K27me3 ChIP-序列化. 这是一个很好的方法.
- ATAC-序列化. ATAC-序列化. ATAC-序列化. ATAC-序列化. ATAC-序列化. ATAC-序列化. ATAC-序列化. ATAC-序列化.
- 进行RNA测序.
主要成果:
- Bmi1 枯竭会改变控制细胞增殖,衰老和死亡的基因.
- 观察到染色质可访问性增加和基因上调.
- 减少H3K27me3丰富与基因变化相关.
- Cdkn2c (细胞循环调节器) 显著上调.
- 抑制Cdkn2c可以挽救内耳上皮细胞的增殖.
结论:
- Bmi1通过H3K27me3.3.保持耳转录抑制.
- Bmi1 枯竭导致 Cdkn2c 过度表达和增殖受损.
- Cdkn2c通路是头发细胞损失和听力损失的潜在治疗点.
更多相关视频
10:28Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
Published on: September 20, 2018
10:09Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
Published on: January 26, 2018
相关概念视频
Inheritance of Chromatin Structures
Chromatin Modification in iPS Cells
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
Epigenetic Regulation
X-chromosome...
Epigenetic Regulation
Genomic Imprinting and Inheritance
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
Spreading of Chromatin Modifications
Writers
The writer...
