Sollerbrant K, Akusjärvi G, Svensson C
Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
J Virol. 1993 Jul;67(7):4195-204. doi: 10.1128/JVI.67.7.4195-4204.1993.
Adenovirus E1A encodes two major proteins of 289 and 243 amino acids (289R and 243R), which both have transcription regulatory properties. E1A-289R is a transactivator whereas E1A-243R primarily functions as a repressor of transcription. Here we show that E1A repression is not restricted to RNA polymerase II genes but also includes the adenovirus virus-associated (VA) RNA genes. These genes are transcribed by RNA polymerase III and have previously been suggested to be the target of an E1A-289R-mediated transactivation. Surprisingly, we found that during transient transfection both E1A proteins repressed VA RNA transcription. E1A repression of VA RNA transcription required both conserved regions 1 and 2 and therefore differed from the E1A-mediated inhibition of simian virus 40 enhancer activity which primarily required conserved region 1. The repression was counteracted by the E1B-19K protein, which also, in the absence of E1A, enhanced the accumulation of VA RNA. Importantly, we show that efficient VA RNA transcription requires expression of both E1A and the E1B-19K protein during virus infection.
腺病毒E1A编码两种主要蛋白质，分别含289个和243个氨基酸（289R和243R），二者均具有转录调控特性。E1A - 289R是一种反式激活因子，而E1A - 243R主要作为转录抑制因子发挥作用。在此我们表明，E1A介导的抑制作用不仅限于RNA聚合酶II基因，还包括腺病毒病毒相关（VA）RNA基因。这些基因由RNA聚合酶III转录，此前有人提出它们是E1A - 289R介导的反式激活作用的靶点。令人惊讶的是，我们发现在瞬时转染过程中，两种E1A蛋白均抑制VA RNA转录。E1A对VA RNA转录的抑制作用需要保守区域1和2，因此不同于E1A介导的对猿猴病毒40增强子活性的抑制作用，后者主要需要保守区域1。这种抑制作用可被E1B - 19K蛋白抵消，在没有E1A的情况下，E1B - 19K蛋白也能增强VA RNA的积累。重要的是，我们表明在病毒感染期间，高效的VA RNA转录需要E1A和E1B - 19K蛋白的共同表达。
