Natural loss‐of‐function mutation of EDR1 conferring resistance to tomato powdery mildew in A rabidopsis thaliana accession C24

To screen for potentially novel types of resistance to tomato powdery mildew O idium neolycopersici , a disease assay was performed on 123 A rabidopsis thaliana accessions. Forty accessions were fully resistant, and one, C24 , was analysed in detail. By quantitative trait locus ( QTL ) analysis of a...

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Veröffentlicht in:Molecular plant pathology 2015-01, Vol.16 (1), p.71-82
Hauptverfasser: Gao, Dongli, Appiano, Michela, Huibers, Robin P., Loonen, Annelies E. H. M., Visser, Richard G. F., Wolters, Anne‐Marie A., Bai, Yuling
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Sprache:eng
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Zusammenfassung:To screen for potentially novel types of resistance to tomato powdery mildew O idium neolycopersici , a disease assay was performed on 123 A rabidopsis thaliana accessions. Forty accessions were fully resistant, and one, C24 , was analysed in detail. By quantitative trait locus ( QTL ) analysis of an F 2 population derived from C24 × S ha (susceptible accession), two QTL s associated with resistance were identified in C24 . Fine mapping of QTL ‐1 on chromosome 1 delimited the region to an interval of 58 kb encompassing 15 candidate genes. One of these was Enhanced Disease Resistance 1 ( EDR1 ). Evaluation of the previously obtained edr1 mutant of Arabidopsis accession Col‐0, which was identified because of its resistance to powdery mildew G olovinomyces cichoracearum , showed that it also displayed resistance to O . neolycopersici . Sequencing of EDR1 in our C24 germplasm (referred to as C24 ‐ W ) revealed two missing nucleotides in the second exon of EDR1 resulting in a premature stop codon. Remarkably, C24 obtained from other laboratories does not contain the EDR1 mutation. To verify the identity of C24 ‐ W , a DNA region containing a single nucleotide polymorphism ( SNP ) unique to C24 was sequenced showing that C24 ‐ W contains the C24 ‐specific nucleotide. C24 ‐ W showed enhanced resistance to O . neolycopersici compared with C24 not containing the edr1 mutation. Furthermore, C24 ‐ W displayed a dwarf phenotype, which was not associated with the mutation in EDR1 and was not caused by the differential accumulation of pathogenesis‐related genes. In conclusion, we identified a natural edr1 mutant in the background of C24 .
ISSN:1464-6722
1364-3703
DOI:10.1111/mpp.12165