Co‐operative autoregulation of a replication protein gene
Co‐operative autoregulation of a replication protein gene
复制标题
复制蛋白基因的协同自动调节
DOI：
10.1111/j.1365-2958.1991.tb01861.x
复制
发表时间：
1991
影响因子：
3.6
通讯作者：
J. H. Crosa
中科院分区：
文献类型：
--
作者：
A. Gammie;J. H. Crosa
在这项工作中，我们介绍了 repi 启动子 (Prepl) 的定位和表征，并展示了调控的各个方面。 Prepl 与其他自动调节复制蛋白基因启动子的比较揭示了相似性，但 Prepl 与其中一些特征启动子的不同之处在于不受热休克 RNA 聚合酶的调节。引物延伸分析表明，Prepl 包含在 5 个螺旋排列的 18 碱基对重复序列中，或者先前定义的最小起源的 18 聚体中。此外，我们发现 Prepl 受到 REPI 区域编码的反式作用产物的自动调节。纯化的 Repl 蛋白与起始点的 18 聚体区域结合，表明 repl 基因受到蛋白产物的自动调节。自动调节似乎是合作性的，因为减少 18 聚体结合位点区域会导致自动抑制的伴随非线性损失。与含有所有结合区域的原始DNA相比，缺失衍生物显示出结合Repl蛋白的能力降低。各种缺失衍生物在体外结合Repl的能力减弱与体内观察到的自抑制的丧失相关。
In this work we present the localization and characterization of the repi promoter (Prepl) and show aspects of the regulation. Comparison of Prepl with other autoregulated replication protein gene promoters revealed similarities, but Prepl differs from some of these characterized promoters in not being regulated by the heat‐shock RNA polymerase. Primer extension analysis showed that Prepl is contained within five helically aligned 18 base pair repeats, or 18‐mers of the previously defined minimal origin. In addition, we find that Prepl is autoregulated by a trans‐acting product encoded in the REPI region. Purified Repl protein binds to the 18‐mer region of the origin, suggesting that the repl gene is autoregulated by the protein product. The autoregutation appears to be co‐operative since decreasing the 18‐mer binding site region results in a concomitant non‐linear loss of auto‐repression. The deletion derivatives show a decreased ability to bind the Repl protein when compared with origin DNA containing all of the binding region. The diminished capacity of the various deletion derivatives to bind Repl in vitro correlates with the loss of autorepression seen in vivo.
DOI：
10.1073/pnas.82.9.2679
发表时间：
1985-01-01
影响因子：
11.1
作者：
COWING, DW;BARDWELL, JCA;GROSS, CA
通讯作者：
GROSS, CA
质粒pSC101的复制起始蛋白是其自身顺反子的转录抑制蛋白。
DOI：
10.1073/pnas.82.8.2252
发表时间：
1985
影响因子：
11.1
作者：
Vocke,C;Bastia,D
通讯作者：
Bastia,D