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监管ISWI涉及阻断模块与核体表皮质对抗

Cedric R Clapier¹, Bradley R Cairns

¹Howard Hughes Medical Institute and Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA. cedric.clapier@hci.utah.edu

|November 13, 2012

概括

染色体重塑者使用调节区域来控制核细胞的滑动. 新的发现揭示了ISWI重塑器是如何被特定的DNA和基因素信号激活的,确保精确的基因调节.

科学领域:

分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
生物化学生物化学

背景情况:

染色体重塑复合体 (CRCs) 通过调动核细胞组,对基因调节至关重要.
CRCs具有催化ATPase/DNA-转位酶子单元和与核体表位素结合的调节侧边区域.
了解这些侧边区域如何调节CRC活动对于破译基因可访问性至关重要.

研究的目的:

为了确定和描述ISWI-家族染色体重塑器中的新型调节区域.
调查核细胞表位调节ISWI活动的机制.
阐明调节区域和ISWI的催化核心之间的功能关系.

主要方法:

生物化学分析测量ATP水解和DNA转位率.
位点定向的突变发生来破坏或去除Drosophila ISWI中已识别的调节区域 (AutoN和NegC).
核体滑动测定在存在或缺少特定的核体表位 (H4尾巴基本补丁,外核体DNA) 的情况下.

主要成果:

在Drosophila ISWI中发现了两个新的保存调节区域,AutoN和NegC.
自动N负面调节ATP水解,而NegC抑制了水解与DNA转位的合.
移除AutoN和NegC使ISWI能够在独立于激活表位和HSS域的情况下滑动核细胞,模仿SWI/SNF ATPase活动.

结论:

ISWI ATPase催化核心本质上是活跃的,AutoN和NegC作为抑制模块.
核体表位因缓解AutoN和NegC所施加的抑制而促进ISWI活动.
这种机制确保ISWI家族的重塑剂对适当的染色质景观有选择性的作用,有助于染色质重塑剂的专业化.

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