Literature DB >> 28233030

Gene coding for an elongation factor is involved in resistance against powdery mildew in common bean.

Ana Campa1, Juan José Ferreira2.   

Abstract

KEY MESSAGE: Genetic control of the resistance response against powdery mildew in common bean was studied combining genetic, genomic and transcriptomic analyses. A candidate resistance gene in cultivar Porrillo Sintetico was proposed. The species causing the fungal disease powdery mildew (PM) in the local common bean crop was identified as Erysiphe polygoni through the molecular analysis of the internal transcribed spacer region. A genetic analysis of the resistance in cultivar Porrillo Sintetico was conducted using different F2:3 populations, and a dominant gene conferring total resistance against a local PM isolate was physically located between 84,188 and 218,664 bp of chromosome Pv04. An in silico analysis of this region, based on the common bean reference sequence, revealed four genes candidate to be involved in the resistance reaction. Relative expression levels of these genes after PM infection showed a significant over-expression of the candidate gene Phvul.004G001500 in the resistant genotype Porrillo Sintetico. This gene was re-sequenced in the parental genotypes X2776 and Porrillo Sintetico to explain their different phenotypic responses against PM. Several substitutions where identified in exon regions, all of them synonymous, so differences in the produced amino acid sequence were not expected. However, a total of 37 mutations were identified in non-coding regions of the gene sequence, suggesting that intron variation could be responsible for the different gene expression levels after PM infection. No evidence of other regulatory mechanisms, such as alternative splicing or methylation, was identified. Candidate resistance gene Phvul.004G001500 codes for an elongation factor that is not a typical gene related to recognition of specific pathogens in plants, suggesting its involvement in the resistance through plant immune system.

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Year:  2017        PMID: 28233030     DOI: 10.1007/s00122-017-2864-x

Source DB:  PubMed          Journal:  Theor Appl Genet        ISSN: 0040-5752            Impact factor:   5.699


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