Staal Jens, Kaliff Maria, Bohman Svante, Dixelius Christina
Department of Plant Biology and Forest Genetics, Swedish University of Agricultural Sciences, Dag Hammarskjölds väg 181, PO Box 7080, 750 07 Uppsala, Sweden.
Plant J. 2006 Apr;46(2):218-30. doi: 10.1111/j.1365-313X.2006.02688.x.
In a cross between the two resistant accessions Col-0 and Ler-0, a 15:1 segregation was found in F2, suggesting the presence of unlinked resistance loci to Leptosphaeria maculans. One hundred Col-4 x Ler-0, and 50 Ler-2 x Cvi-1 recombinant inbred lines, and seven susceptible Ler-0 x Ws-0 F2 progenies were examined to identify the two loci. Resistance in Col-4, Ws-0 and Cvi-1 (RLM1) was mapped to the marker m305 on chromosome 1. Col-4 x Ler-0 and Ler-2 x Cvi-1 mapping populations located RLM2(Ler) on the same arm of chromosome 4. A tight physical location of RLM2 was established through near-isogenic lines. This region was found to correspond to an ancient duplication event between the RLM1 and RLM2 loci. Two independent T-DNA mutants in a TIR-NB-LRR R gene (At1g64070) displayed susceptibility, and L. maculans susceptible mutant phenotypes were confirmed to be allelic for rlm1 in F1 after crosses with susceptible rlm1(Ler)rlm2(Col) plants. Complementation of rlm1(Ler)rlm2(Col) with the genomic Col-0 sequence of At1g64070 conferred resistance. In addition, two T-DNA mutants in a neighbouring homologous TIR-NB-LRR gene (At1g63880) displayed moderate susceptibility to L. maculans. Sequence analysis revealed that At1g64070 was truncated by a premature stop codon, and that At1g63880 was absent in Ler-0. RNA interference confirmed that Ler-0 resistance is dependent on genes structurally related to RLM1. Camalexin was identified as a quantitative co-dominant resistance factor of Col-0 origin, but independent of RLM1. RLM1/RLM2 resistance was, however, found to require RAR1 and partially HSP90.1.
在两个抗性材料Col-0和Ler-0的杂交中，F2代出现了15:1的分离比例，这表明存在与黄斑盘多毛孢菌不连锁的抗性位点。研究人员检测了100个Col-4×Ler-0和50个Ler-2×Cvi-1重组自交系，以及7个感病的Ler-0×Ws-0 F2代子代，以确定这两个位点。Col-4、Ws-0和Cvi-1（RLM1）中的抗性被定位到第1号染色体上的标记m305处。Col-4×Ler-0和Ler-2×Cvi-1的定位群体将RLM2（Ler）定位在第4号染色体的同一臂上。通过近等基因系确定了RLM2的紧密物理位置。发现该区域对应于RLM1和RLM2位点之间的一个古老重复事件。一个TIR-NB-LRR R基因（At1g64070）中的两个独立T-DNA突变体表现出感病性，并且在与感病的rlm1（Ler）rlm2（Col）植株杂交后，F1代中黄斑盘多毛孢菌感病突变体表型被确认为与rlm1等位。用At1g64070的Col-0基因组序列对rlm1（Ler）rlm2（Col）进行互补可赋予抗性。此外，一个相邻同源TIR-NB-LRR基因（At1g63880）中的两个T-DNA突变体对黄斑盘多毛孢菌表现出中度感病性。序列分析表明，At1g64070因一个提前的终止密码子而截短，并且At1g63880在Ler-0中不存在。RNA干扰证实Ler-0的抗性依赖于与RLM1结构相关的基因。植保素被鉴定为一个源自Col-0的数量共显性抗性因子，但与RLM1无关。然而，发现RLM1/RLM2抗性需要RAR1和部分HSP90.1。
