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首页> 外文期刊>Molecular and Cellular Biology >Elements in the immunoglobulin heavy-chain enhancer directly regulate simian virus 40 ori-dependent DNA replication.
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Elements in the immunoglobulin heavy-chain enhancer directly regulate simian virus 40 ori-dependent DNA replication.

机译：免疫球蛋白重链增强剂中的元素直接调节猿猴病毒40 ori依赖性DNA复制。

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摘要

In a previous study, we showed that the immunoglobulin heavy-chain (IgH) enhancer (IgHe) is near or in an initiation zone of chromosomal DNA replication, which is preferentially active in B cells (K. Ariizumi, Z. Wang, and P. W. Tucker, Proc. Natl. Acad. Sci. USA 90:3695-3699, 1993). This suggests the existence of a functional relationship between IgHe-mediated transcription and DNA replication. To test this theory, we utilized simian virus 40 (SV40) DNA replication as a model of chromosomal replication. IgHe or its operationally divisible domains (5'-En, core, and 3'-En) were introduced into SV40 minichromosomes (IgHe-SV40). Results of replication assays with IgHe-SV40 replicons indicated that the 5'-En and 3'-En activated or suppressed SV40 DNA replication regardless of the presence of SV40 enhancers or promoters in these replicons. The activity did not reside in IgHe core sequences. The results suggested that the 5'- and 3'-En regulated SV40 replication through direct interaction with the origin, not through suppression at the SV40 enhancer and/or promoter. In an effort to identify elements within the 5'-En motif that contributed to this effect, we found that the E site, but not microE5 and microE2 boxes, upregulated DNA replication. Our results provide another possible regulatory function for the 5'-En and 3'-En domains besides transcriptional suppression of IgHe.
机译：在先前的研究中，我们表明免疫球蛋白重链（IgH）增强子（IgHe）在染色体DNA复制的起始区域附近或之中，该区域在B细胞中优先活跃（K. Ariizumi，Z。Wang和PW Tucker，Proc.Natl.Acad.Sci.USA 90：3695-3699，1993）。这表明IgHe介导的转录和DNA复制之间存在功能关系。为了验证该理论，我们利用猿猴病毒40（SV40）DNA复制作为染色体复制的模型。将IgHe或其可操作的可划分域（5'-En，核心和3'-En）引入SV40微型染色体（IgHe-SV40）。用IgHe-SV40复制子进行复制测定的结果表明，无论这些复制子中是否存在SV40增强子或启动子，5'-En和3'-En均可激活或抑制SV40 DNA复制。该活性不存在于IgHe核心序列中。结果表明5'-和3'-En通过与原点的直接相互作用而不是通过在SV40增强子和/或启动子处的抑制来调节SV40复制。为了确定5'-En基序中促成此效应的元素，我们发现E位点（而非microE5和microE2盒）上调了DNA复制。我们的研究结果为IgHe的转录抑制提供了5'-En和3'-En结构域的另一种可能的调节功能。

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