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Collaborative Competition Mechanism for Gene Activation In Vivo

机译：体内基因激活的协同竞争机制

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摘要

The mechanism by which gene regulatory proteins gain access to their DNA target sites is not known. In vitro, binding is inherently cooperative between arbitrary DNA binding proteins whose target sites are located within the same nucleosome. We refer to such competition-based cooperativity as collaborative competition. Here we show that arbitrarily chosen foreign DNA binding proteins, LexA and Tet repressor, cooperate with an adjacently binding endogenous activator protein, Gcn4, to coactivate expression of chromosomal reporter genes in Saccharomyces cerevisiae. Coactivation requires that the cooperating target sites be within a nucleosome-length distance; it leads to increased occupancy by Gcn4 at its binding site; and it requires both Gcn5 and Swi/Snf which, at an endogenous Gcn4-dependent promoter, act subsequent to Gcn4 binding. These results imply that collaborative competition contributes to gene regulation in vivo. They further imply that, even in the presence of the cell's full wild-type complement of chromatin remodeling factors, competition of regulatory proteins with histone octamer for access to regulatory target sites remains a quantitative determinant of gene expression levels. We speculate that initial target site recognition and binding may occur via spontaneous nucleosomal site exposure, with remodeling factor action required downstream to lock in higher levels of regulatory protein occupancy.
机译：基因调节蛋白接近其DNA靶位点的机制尚不清楚。在体外， 结合是目标位置位于同一核小体中的任意DNA结合蛋白之间的固有协同作用。我们将这种基于竞争的合作称为协作竞争。在这里，我们显示了任意选择的外源DNA结合蛋白LexA和Tet阻遏物，与相邻结合的内源性激活蛋白Gcn4协同作用，共同激活了酿酒酵母中的染色体报告基因表达。共激活要求合作的靶位点在核小体长度距离之内。它导致Gcn4在其结合位点的占用增加;它需要Gcn5和Swi / Snf两者，它们在内源性Gcn4依赖性启动子上，在Gcn4结合后起作用。这些结果暗示协同竞争有助于体内基因调控。他们进一步暗示，即使存在染色质重塑因子的完整野生型补体，调节蛋白与组蛋白八聚体竞争进入调节靶位点的竞争仍是基因表达水平的定量决定因素。我们推测，最初的靶位点识别和结合可能通过自发的核小体位点暴露而发生，下游需要重塑因子作用以锁定更高水平的调节蛋白占有率。

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