Present address: Department of Medical Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Dag Hammarskjölds väg 20, 751 85 Uppsala, Sweden.
Transgressive segregation reveals two Arabidopsis TIR-NB-LRR resistance genes effective against Leptosphaeria maculans, causal agent of blackleg disease
Article first published online: 21 MAR 2006
The Plant Journal
Volume 46, Issue 2, pages 218–230, April 2006
How to Cite
Staal, J., Kaliff, M., Bohman, S. and Dixelius, C. (2006), Transgressive segregation reveals two Arabidopsis TIR-NB-LRR resistance genes effective against Leptosphaeria maculans, causal agent of blackleg disease. The Plant Journal, 46: 218–230. doi: 10.1111/j.1365-313X.2006.02688.x
- Issue published online: 21 MAR 2006
- Article first published online: 21 MAR 2006
- Received 4 October 2005; revised 30 November 2005; accepted 8 December 2005.
- complex trait;
- natural variation;
- R gene signalling
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 × Ler-0, and 50 Ler-2 × Cvi-1 recombinant inbred lines, and seven susceptible Ler-0 × 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 × Ler-0 and Ler-2 × Cvi-1 mapping populations located RLM2Ler 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 rlm1Lerrlm2Col plants. Complementation of rlm1Lerrlm2Col 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.