Positive and negative regulation of chicken anemia virus transcription.
Positive and negative regulation of chicken anemia virus transcription.
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鸡贫血病毒转录的正向和负向调节。
DOI：
10.1128/jvi.79.5.2859-2868.2005
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Schat,KarelA
中科院分区：
文献类型：
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作者：
Miller,MyrnaM;Jarosinski,KeithW;Schat,KarelA
鸡贫血病毒（chicken anemia virus，CAV）是一种小型环状单链DNA病毒，具有一个启动子-增强子区域，包含四个与雌激素反应元件（estrogen response element，ERE）共有半位点（A）GGTCA相似的共有环腺苷酸反应元件序列（AGCTCA）。这些序列被排列为直接重复序列，这种排列可以被核受体超家族的成员识别。瞬时转染试验使用短CAV启动子构建体，其终止于转录起始位点并驱动增强型绿色荧光蛋白（EGFP）的表达，在DF-1、LMH、LMH/2A以及初级卵泡膜细胞和颗粒细胞中显示出高的基础活性。雌激素受体增强的细胞系，LMH/2A，有显着更大的表达比LMH细胞，这种表达与雌激素治疗显着增加。发现在第一CAV蛋白翻译起始位点下游包括GGTCA样序列的长启动子构建体在DF-1细胞中的EGFP表达显著低于短启动子，这主要是由于RNA转录降低。DNA-蛋白质结合试验表明，蛋白质识别的共识ERE回文也结合GGTCA样序列的CAV启动子。雌激素受体和核受体超家族的其他成员可能提供了一种机制，在低病毒拷贝数的情况下调节CAV的活性。
Chicken anemia virus (CAV) is a small circular single-stranded DNA virus with a single promoter-enhancer region containing four consensus cyclic AMP response element sequences (AGCTCA), which are similar to the estrogen response element (ERE) consensus half-sites (A)GGTCA. These sequences are arranged as direct repeats, an arrangement that can be recognized by members of the nuclear receptor superfamily. Transient-transfection assays which use a short CAV promoter construct that ended at the transcription start site and drive expression of enhanced green fluorescent protein (EGFP) showed high basal activity in DF-1, LMH, LMH/2A, and primary theca and granulosa cells. The estrogen receptor-enhanced cell line, LMH/2A, had significantly greater expression than LMH cells, and this expression was significantly increased with estrogen treatment. A long promoter construct which included GGTCA-like sequences downstream of the first CAV protein translation start site was found to have significantly less EGFP expression in DF-1 cells than the short promoter, which was largely due to decreased RNA transcription. DNA-protein binding assays indicated that proteins recognizing a consensus ERE palindrome also bind GGTCA-like sequences in the CAV promoter. Estrogen receptor and other members of the nuclear receptor superfamily may provide a mechanism to regulate CAV activity in situations of low virus copy number.