Shung Chia-Yi, Sunter Garry
Department of Biology, The University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249, USA.
Virology. 2007 Jul 20;364(1):112-22. doi: 10.1016/j.virol.2007.03.006. Epub 2007 Apr 3.
Studies using Nicotiana benthamiana protoplasts have determined that repression of upstream transcription by AL1 protein enhances AL2 and AL3 expression in Tomato golden mosaic virus (TGMV). Mutations resulting in the inability of TGMV AL1 protein to associate with its cognate binding site, result in a decrease in both AL2 and AL3 expression. Reduced expression correlates with an increase in transcription from the AL62 start site, and decreased transcription from downstream initiation sites (AL1935 and AL1629) present within the AL1 coding region. The results demonstrate that, in a tobacco protoplast system, repression of AL62 transcription, regulated through binding of AL1 protein to sequences in the origin of replication, is required prior to AL2 and AL3 gene expression from the AL1935 and AL1629 viral transcripts. This provides a mechanism to regulate expression of AL2, which is involved in suppression of host defense responses and is required for late gene expression.
利用本氏烟草原生质体进行的研究已确定，番茄金花叶病毒（TGMV）中AL1蛋白对上游转录的抑制会增强AL2和AL3的表达。导致TGMV AL1蛋白无法与其同源结合位点结合的突变，会导致AL2和AL3表达均下降。表达降低与AL62起始位点转录增加以及AL1编码区域内下游起始位点（AL1935和AL1629）转录减少相关。结果表明，在烟草原生质体系统中，在通过AL1935和AL1629病毒转录本表达AL2和AL3基因之前，需要通过AL1蛋白与复制起点序列的结合来抑制AL62转录。这提供了一种调节AL2表达的机制，AL2参与宿主防御反应的抑制，并且是晚期基因表达所必需的。
