Noreen Faiza, Akbergenov Rashid, Hohn Thomas, Richert-Pöggeler Katja R
Friedrich Miescher Institute, Maulbeerstlasse 66, CH-4058 Basel, Switzerland.
Plant J. 2007 Apr;50(2):219-29. doi: 10.1111/j.1365-313X.2007.03040.x.
Endogenous viruses exist in all kingdoms. They usually have active mechanisms of integration, as in bacteriophage lambda and animal retroviruses, and sophisticated mechanisms to maintain a proviral state over decades and generations. Plant para retroviruses, however, neither have an integrase, nor genes for maintaining the proviral state. How are those elements controlled, and under what conditions can they be activated? Here we study the proviral state of endogenous petunia vein clearing virus (ePVCV). Our results support the hypothesis that the proviral state is associated with a host silencing mechanism manifested by DNA methylation, chromatin modification and production of small interfering (si) RNAs. PVCV may be induced by applying abiotic stress, leading to the development of viral symptoms and increased transcript and siRNA levels. Similar levels of ePVCV DNA methylation were observed in two different lines of Petunia hybrida, RdC (rose du ciel) and W138, the latter known for its active version of transposon dTph1. In contrast, significant differences in histone modification were detected. The predominant association of ePVCV sequences with histone H3 methylated at lysine 9 (H3mK9) in RdC and with about equal amounts of H3mK9 and H3mK4 in W138 indicates a less repressive proviral state in the latter cultivar.
内源性病毒存在于所有生物界。它们通常具有活跃的整合机制，如在λ噬菌体和动物逆转录病毒中，以及复杂的机制来维持数十年和几代人的前病毒状态。然而，植物类逆转录病毒既没有整合酶，也没有维持前病毒状态的基因。这些元件是如何被控制的，在什么条件下它们会被激活？在这里，我们研究了矮牵牛脉明病毒（ePVCV）的前病毒状态。我们的结果支持这样一种假设，即前病毒状态与宿主沉默机制相关，这种机制表现为DNA甲基化、染色质修饰和小干扰（si）RNA的产生。通过施加非生物胁迫可能诱导PVCV，导致病毒症状的出现以及转录本和siRNA水平的增加。在两种不同的矮牵牛品系RdC（玫瑰天空）和W138中观察到相似水平的ePVCV DNA甲基化，后者以其活跃的转座子dTph1版本而闻名。相比之下，检测到组蛋白修饰存在显著差异。在RdC中，ePVCV序列与赖氨酸9甲基化的组蛋白H3（H3mK9）主要相关，而在W138中，H3mK9和H3mK4的量大致相等，这表明后一个品种中的前病毒状态抑制性较小。
