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奇克1是一种素H3三氨酸11激酶,它调节DNA损伤诱导的转录抑制
Midori Shimada1, Hiroyuki Niida, Doaa H Zineldeen
1Department of Cell Biology and Biochemistry, Graduate School of Medical Sciences, Nagoya City University, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.
Cell
|February 5, 2008
概括
DNA损伤迅速降低了基因组H3氨酸11酸化,抑制了像环林B1这样的基因. 这涉及Chk1与染色质的解离,减少基因素乙化和基因转录.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- DNA损伤会引发复杂的基因表达变化,包括转录激活和抑制.
- 与激活通路相比,基因损伤诱导的转录抑制背后的机制仍然不太清楚.
研究的目的:
- 为了研究基因组修饰在DNA损伤诱导的转录抑制中的作用.
- 阐明Chk1激酶参与调节基因表达后DNA损伤的作用.
主要方法:
- 在DNA损伤后对基因素H3氨酸11 (H3-T11) 酸化动态的分析.
- 评估Chk1激酶活性和染色体协会.
- 染色体免疫沉以评估素乙化和转录因子对基因促进体的结合.
主要成果:
- DNA损伤迅速减少H3-T11酸化,与抑制诸如cyclin B1和cdk1.1等基因相关.
- H3-T11酸化依赖于细胞周期,并由Chk1.1调节.
- 在DNA受损时,Chk1与染色质分离,导致H3-T11酸化降低,并降低了基因素乙烯转移酶GCN5结合.
- H3-T11酸化的丧失与目标基因促进体的H3-K9乙化减少有关.
结论:
- Chk1 作为基因素激酶,调解DNA损伤诱导的转录抑制.
- 该机制涉及Chk1-依赖的H3-T11酸化和随后的素乙化损失.
- 这项研究揭示了针对DNA损伤的基因表达的表观遗传调节的新途径.
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