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甲基化模式在PAP调节DNA控制中皮埃龙炎相关的E. coli中的 pili阶段变化

B A Braaten¹, X Nou, L S Kaltenbach

¹Department of Pathology, University of Utah Health Sciences Center, Salt Lake City 84132.

|February 11, 1994

概括

在大肠杆菌中,DNA甲基化模式调节了与烟炎相关的 pili (Pap) 表达. 在GATC1028的甲基化抑制了Pap ON状态,而在GATC1130的甲基化是必要的.

科学领域:

微生物学微生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
细菌遗传学细菌遗传学

背景情况:

在大肠杆菌中,与白炎相关的 pili (Pap) 表达表现呈现相位变化,在 ON 和 OFF 状态之间切换.
通过Dam甲基转移酶在特定GATC位点的DNA甲基化影响了这种相变化.

研究的目的:

研究DNA甲基化在GATC1028和GATC1130在调节Pap ON/OFF相变化的特定作用.
阐明这些部位的甲基化影响调节性蛋白质结合和基因表达的分子机制.

主要方法:

针对GATC1028和GATC1130的局部导向突变发生,以防止甲基化.
对野生型和突变大肠杆菌菌株的帕普相变异的分析.
电泳运动转移试验 (EMSAs) 用于评估蛋白质-DNA相互作用.

主要成果:

甲基化GATC1028通过抑制Lrp和Papi结合来阻止ON状态.
甲基化GATC1130对于ON状态至关重要,可能通过阻断靠近pilin促进体的LRP结合.
这些位点的突变改变了正常的相变异模式.

结论:

特定GATC位点的DNA甲基化是E. coli中Pap ON/OFF切换的关键调节者.
GATC1028和GATC1130的微分甲基化通过调节调节蛋白相互作用来决定相位状态.
提出了一种在Pap ON和OFF状态之间以甲基化驱动的过渡模型.

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