Kwon Soon Il, Koczan Jessica M, Gassmann Walter
Department of Plant Microbiology and Pathology, University of Missouri-Columbia, Columbia, MO 65211-7140, USA.
Plant J. 2004 Nov;40(3):366-75. doi: 10.1111/j.1365-313X.2004.02213.x.
RPS4 specifies the Arabidopsis disease resistance response to Pseudomonas syringae pv. tomato expressing avrRps4 and was cloned based on the identification of RLD as a naturally occurring susceptible accession. To dissect the molecular and genetic basis of disease resistance, we used a genetic approach to identify suppressor mutations that reactivate the avrRps4-triggered defense response in RLD. In this report, we describe two non-allelic srfr (suppressor of rps4-RLD) mutants, srfr1 and srfr3, that were susceptible to virulent P. syringae pv. tomato strain DC3000, but resistant to DC3000 expressing avrRps4. In quantitative bacterial growth assays, growth of DC3000 was similar in wild-type control and both mutant lines, indicating that basal resistance was not enhanced in srfr1 and srfr3. Growth of DC3000 (avrRps4) was approximately 30-fold lower in srfr1 and srfr3 than in RLD, but intermediate compared with fully resistant Col-0 and transgenic RLD containing RPS4-Col. The srfr1 and srfr3 mutants did not develop spontaneous lesions prior to inoculation or constitutively express the pathogenesis-related gene PR-1. Therefore, srfr1 and srfr3 constitute novel avr-specific mutants that differ from previously described Arabidopsis mutants with elevated disease resistance. The srfr1 and srfr3 mutations were recessive, and both mapped to the bottom of chromosome IV. Genetic analysis indicated that resistance in srfr1 and srfr3 was independent of the rps4-RLD allele, but dependent on a second gene in RLD. We propose that SRFR1 and SRFR3 are negative regulators of avrRps4-triggered gene-for-gene disease resistance.
RPS4决定了拟南芥对表达avrRps4的丁香假单胞菌番茄致病变种的抗病反应，它是基于将RLD鉴定为天然存在的感病种质而克隆得到的。为了剖析抗病性的分子和遗传基础，我们采用遗传方法来鉴定能在RLD中重新激活avrRps4触发的防御反应的抑制突变。在本报告中，我们描述了两个非等位的srfr（rps4-RLD的抑制子）突变体srfr1和srfr3，它们对毒性较强的丁香假单胞菌番茄致病变种DC3000敏感，但对表达avrRps4的DC3000具有抗性。在定量细菌生长测定中，DC3000在野生型对照和两个突变系中的生长情况相似，这表明srfr1和srfr3中基础抗性并未增强。在srfr1和srfr3中，DC3000（avrRps4）的生长比在RLD中低约30倍，但与完全抗性的Col-0和含有RPS4-Col的转基因RLD相比处于中间水平。srfr1和srfr3突变体在接种前未出现自发损伤，也未组成型表达病程相关基因PR-1。因此，srfr1和srfr3构成了新的avr特异性突变体，与先前描述的具有增强抗病性的拟南芥突变体不同。srfr1和srfr3突变是隐性的，且都定位在第四条染色体的底部。遗传分析表明，srfr1和srfr3中的抗性独立于rps4-RLD等位基因，但依赖于RLD中的另一个基因。我们推测SRFR1和SRFR3是avrRps4触发的基因对基因抗病性的负调控因子。
