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首页> 外文期刊>Journal of bacteriology >Dimers of π Protein Bind the A+T-Rich Region of the R6K γ Origin near the Leading-Strand Synthesis Start Sites: Regulatory Implications
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Dimers of π Protein Bind the A+T-Rich Region of the R6K γ Origin near the Leading-Strand Synthesis Start Sites: Regulatory Implications

机译：π蛋白的二聚体与前导链合成起始位点附近的R6Kγ起源的A + T富集区结合：调控意义。

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The replication of γ origin, a minimal replicon derived from plasmid R6K, is controlled by the Rep protein π. At low intracellular concentrations, π activates the γ origin, while it inhibits replication at elevated concentrations. Additionally, π acts as a transcription factor (auto)repressing its own synthesis. These varied regulatory functions depend on π binding to reiterated DNA sequences bearing a TGAGNG motif. However, π also binds to a “non-iteron” site (i.e., not TGAGNG) that resides in the A+T-rich region adjacent to the iterons. This positioning places the non-iteron site near the start sites for leading-strand synthesis that also occur in the A+T-rich region of γ origin. We have hypothesized that origin activation (at low π levels) would require the binding of π monomers to iterons, while the binding of π dimers to the non-iteron site (at high π levels) would be required to inhibit priming. Although monomers as well as dimers can bind to an iteron, we demonstrate that only dimers bind to the non-iteron site. Two additional pieces of data support the hypothesis of negative replication control by π binding to the non-iteron site. First, π binds to the non-iteron site about eight times less well than it binds to a single iteron. Second, hyperactive variants of π protein (called copy-up) either do not bind to the non-iteron site or bind to it less well than wild-type π. We propose a replication control mechanism whereby π would directly inhibit primer formation.
机译：γ起点的复制是从质粒R6K衍生的最小复制子，由Rep蛋白π控制。在低细胞内浓度下，π激活γ起源，而在高浓度下则抑制复制。另外，π充当转录因子（自动）抑制其自身的合成。这些不同的调节功能取决于与具有TGAGNG基序的重复DNA序列的π结合。然而，π也结合到位于与迭代子相邻的富含A + T的区域中的“非-子”位点（即，不是TGAGNG）。这种定位将非铁原子位点放置在前导链合成的起始位点附近，该起始位点也发生在γ源的富含A + T的区域。我们假设起源激活（低π水平）将要求π单体与Iteron结合，而π二聚体与非铁原子位点（高π水平）的结合需要抑制引发。尽管单体以及二聚体都可以与一个Iteron结合，但我们证明只有二聚体与非Itron的位点结合。另外两个数据通过π绑定到非子位点支持负复制控制的假设。首先，π结合到非子位点的能力比结合单个Iteron少八倍。其次，π蛋白的高活性变体（称为复制）要么不与非子位点结合，要么与野生型π结合得不太好。我们提出了一种复制控制机制，其中π将直接抑制引物形成。

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