Natural loss‐of‐function mutation of EDR1 conferring resistance to tomato powdery mildew in Arabidopsis thaliana accession C24. (9th July 2014)

• Record Type: Journal Article
• Authors: Gao, Dongli; Appiano, Michela; Huibers, Robin P.; Loonen, Annelies E. H. M.; Visser, Richard G. F.; Wolters, Anne‐Marie A.; Bai, Yuling
• Is Part Of: Molecular plant pathology. Volume 16:Number 1(2015:Jan.)
• Page Start: 71
• Page End: 82
• Publication Date: 2014-07-09
• Subjects: Plant diseases -- Molecular aspects -- Periodicals; Plant-pathogen relationships -- Molecular aspects -- Periodicals; 571.936
• DOI: 10.1111/mpp.12165
• Languages: English
• ISSNs: 1464-6722

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>To screen for potentially novel types of resistance to tomato powdery mildew <italic>Oidium neolycopersici</italic>, a disease assay was performed on 123 <italic>Arabidopsis thaliana</italic> accessions. Forty accessions were fully resistant, and one, C24, was analysed in detail. By quantitative trait locus (QTL) analysis of an F<sub>2</sub> population derived from C24 × Sha (susceptible accession), two QTLs 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 <italic>Enhanced Disease Resistance 1</italic> (<italic>EDR1</italic>). Evaluation of the previously obtained <italic>edr1</italic> mutant of Arabidopsis accession Col‐0, which was identified because of its resistance to powdery mildew <italic>Golovinomyces cichoracearum</italic>, showed that it also displayed resistance to <italic>O. neolycopersici</italic>. Sequencing of <italic>EDR1</italic> in our C24 germplasm (referred to as C24‐W) revealed two missing nucleotides in the second exon of <italic>EDR1</italic> resulting in a premature stop codon. Remarkably, C24 obtained from other laboratories does not contain the <italic>EDR1</italic> 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 <italic>O. neolycopersici</italic> compared with C24 not containing the <italic>edr1</italic> mutation. Furthermore, C24‐W displayed a dwarf phenotype, which was not associated with the mutation in <italic>EDR1</italic> and was not caused by the differential accumulation of pathogenesis‐related genes. In conclusion, we identified a natural <italic>edr1</italic> mutant in the background of C24.</p> </abstract>