Goritschnig Sandra, Zhang Yuelin, Li Xin
Michael Smith Laboratories, Room 301, 2185 East Mall, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.
Plant J. 2007 Feb;49(3):540-51. doi: 10.1111/j.1365-313X.2006.02978.x. Epub 2007 Jan 8.
Plant defences require a multitude of tightly regulated resistance responses. In Arabidopsis, the unique gain-of-function mutant suppressor of npr1-1 constitutive 1 (snc1) carries a point mutation in a Resistance (R)-gene, resulting in constitutive activation of defence responses without interaction with pathogens. This has allowed us to identify various downstream signalling components essential in multiple defence pathways. One mutant that suppresses snc1-mediated constitutive resistance is modifier of snc1 5 (mos5), which carries a 15-bp deletion in UBA1, one of two ubiquitin-activating enzyme genes in Arabidopsis. A mutation in UBA2 does not suppress snc1, suggesting that these two genes are not equally required in Arabidopsis disease resistance. On the other hand, a mos5 uba2 double mutant is lethal, implying partial redundancy of the two homologues. Apart from affecting snc1-mediated resistance, mos5 also exhibits enhanced disease susceptibility to a virulent pathogen and is impaired in response to infection with avirulent bacteria carrying the protease elicitor AvrRpt2. The mos5 mutation in the C-terminus of UBA1 might affect binding affinity of the downstream ubiquitin-conjugating enzymes, thus perturbing ubiquitination of target proteins. Furthermore, SGT1b and RAR1, which are necessary for resistance conferred by the SNC1-related R-genes RPP4 and RPP5, are dispensable in snc1-mediated resistance. Our data reveal the definite requirement for the ubiquitination pathway in the activation and downstream signalling of several R-proteins.
植物防御需要多种严格调控的抗性反应。在拟南芥中，npr1-1组成型1（snc1）的独特功能获得型突变体抑制子在一个抗性（R）基因中携带一个点突变，导致防御反应的组成型激活，而无需与病原体相互作用。这使我们能够鉴定出多种防御途径中必不可少的各种下游信号成分。一个抑制snc1介导的组成型抗性的突变体是snc1 5（mos5）的修饰子，它在拟南芥中两个泛素激活酶基因之一的UBA1中携带15个碱基对的缺失。UBA2中的突变不会抑制snc1，这表明这两个基因在拟南芥抗病性中并非同等必需。另一方面，mos5 uba2双突变体是致死的，这意味着这两个同源物存在部分冗余。除了影响snc1介导的抗性外，mos5对毒性病原体也表现出增强的感病性，并且在对携带蛋白酶激发子AvrRpt2的无毒细菌感染的反应中受损。UBA1 C末端的mos5突变可能会影响下游泛素结合酶的结合亲和力，从而扰乱靶蛋白的泛素化。此外，SGT1b和RAR1是SNC1相关R基因RPP4和RPP5赋予抗性所必需的，但在snc1介导的抗性中是可有可无的。我们的数据揭示了泛素化途径在几种R蛋白的激活和下游信号传导中的明确需求。
