Yang Jun-Yi, Iwasaki Mayumi, Machida Chiyoko, Machida Yasunori, Zhou Xueping, Chua Nam-Hai
Laboratory of Plant Molecular Biology, The Rockefeller University, New York, New York 10065, USA.
Genes Dev. 2008 Sep 15;22(18):2564-77. doi: 10.1101/gad.1682208.
Viruses induce pathogenic symptoms on plants but the molecular basis is poorly understood. Here, we show that transgenic Arabidopsis expressing the pathogenesis protein betaC1 of Tomato yellow leaf curl China virus (TYLCCNV), a geminivirus, can phenocopy to a large extent disease symptoms of virus-infected tobacco plants in having upward curled leaves, radialized leaves with outgrowth tissues from abaxial surfaces, and sterile flowers. These morphological changes are paralleled by a reduction in miR165/166 levels and an increase in PHB and PHV transcript levels. Two factors, ASYMMETRIC LEAVES 1 (AS1) and ASYMMETRIC LEAVES 2 (AS2), are known to regulate leaf development as AS1/AS2 complex. Strikingly, betaC1 plants phenocopy plants overexpressing AS2 at the morphological and molecular level and betaC1 is able to partially complement as2 mutation. betaC1 binds directly to AS1, elicits morphological and gene expression changes dependent on AS1 but not AS2, and attenuates expression of selective jasmonic acid (JA)-responsive gene. Our results show that betaC1 forms a complex with AS1 to execute its pathogenic functions and to suppress a subset of JA responses.
病毒会在植物上引发致病症状，但其分子基础却知之甚少。在此，我们表明，表达双生病毒中国番茄黄化曲叶病毒（TYLCCNV）致病蛋白βC1的转基因拟南芥，在很大程度上可模拟病毒感染烟草植株的病害症状，表现为叶片向上卷曲、叶片呈辐射状且叶背有增生组织以及花朵不育。这些形态变化伴随着miR165/166水平的降低以及PHB和PHV转录本水平的升高。已知两个因子，即不对称叶片1（AS1）和不对称叶片2（AS2），作为AS1/AS2复合体调控叶片发育。引人注目的是，βC1植株在形态和分子水平上模拟了过表达AS2的植株，并且βC1能够部分互补as2突变。βC1直接与AS1结合，引发依赖于AS1而非AS2的形态和基因表达变化，并减弱选择性茉莉酸（JA）响应基因的表达。我们的结果表明，βC1与AS1形成复合体以执行其致病功能并抑制一部分JA反应。
