Abstract
Lr34 in wheat is a non-race-specific gene that confers resistance against multiple fungal pathogens. The resistant allele Lr34 and the susceptible allele Lr34s can be distinguished by three polymorphisms that cause alternation of deduced amino acid sequences of Lr34 at the protein level. In seedlings of a cultivar carrying the resistant Lr34r allele, only a portion (35%) of its transcripts was correctly spliced and the majority (65%) of its transcripts were incorrectly spliced due to multiple mis-splicing events. Lr34 mis-splicing events were also observed at adult plant age when this gene exerts its function. All of the mis-spliced Lr34r cDNA transcripts observed in this study resulted in a premature stop codon due to a shift of the open reading frame; hence, the mis-spliced Lr34r cDNAs were deduced to encode incomplete proteins. Even if a cultivar has a functional Lr34 gene, its transcripts might not completely splice in a correct pattern. These findings suggested that the partial resistance conferred by a quantitative gene might be due to mis-splicing events in its transcripts; hence, the resistance of the gene could be increased by eliminating or mutating regulators that cause mis-splicing events in wheat.
Highlights
Wheat (Triticum aestivum, 2n = 6x = 42, AABBDD) is a major food crop worldwide, but is constantly challenged by several fungal diseases, such as leaf rust and stripe rust [1, 2]
Winter wheat cultivar 2174 that has been experimentally confirmed to have a resistant allele at Lr34-Dr on homoeologous chromosome 7D [22] was used to amplify the complete cDNA of Lr34-Dr At the beginning of the study, no sequence for homoeologous Lr34 genes in common wheat was available, primers Lr34-Exp-F1 and Lr34-Exp-R1 primers used to amplify Lr34r on chromosome 7D were found to amplify Lr34-B that was translocated to homoeologous genome 4A in hexaploid wheat [26]
We examined mis-spliced Lr34 transcripts in adult plants, in which Lr34r exerts its function in resistance to pathogens
Summary
There are numerous genes or quantitative trait loci (QTL) that have been mapped for host plant resistance to epidemic pathogens, including 67 genes/QTL for stripe rust and 69 for leaf rust [3]. The resistance of these genes/QTL can be divided into two types: complete or qualitative resistance, and partial or quantitative resistance [4,5,6,7,8,9,10,11]. Qualitative resistance fits a gene-for-gene model, in which a pathogen is recognized by a plant host resistance gene resulting in complete exclusion of the pathogen [12]. Quantitative resistance remains poorly understood but is explained by two hypotheses: i) a consequence of interactions among multiple resistance genes [13, 14], or ii) the outcome of direct interactions between pathogen effectors and plant defense proteins or indirect interactions between pathogen effectors and plant defense proteins triggered by the effectors [15, 16].
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