��� }�(�data�}��articles�]�(}�(�pmid��33622734��title��PConvergent Adaptation to Quantitative Host Resistance in a Major Plant Pathogen.��authors�]�(�Jean Carlier��François Bonnot��Véronique Roussel��Sébastien Ravel��Reina Teresa Martinez��Luis Perez-Vicente��Catherine Abadie��Stephen Wright�e�journal��mBio��publication_date��2021-Feb��abstract���Plant pathogens can adapt to quantitative resistance, eroding its effectiveness. The aim of this work was to reveal the genomic basis of adaptation to such a resistance in populations of the fungus ��doi��10.1128/mBio.03129-20��
mesh_terms�]�(�Adaptation, Physiological��
Ascomycota��Genome, Bacterial��Host-Pathogen Interactions��Musa��Plant Diseases�eu}�(h�34845779�h�nComplex adaptive architecture underlies adaptation to quantitative host resistance in a fungal plant pathogen.�h
]�(�Thomas Dumartinet��Sébastien Ravel��Véronique Roussel��Luis Perez-Vicente��Jaime Aguayo��Catherine Abadie��Jean Carlier�eh�Molecular ecology�h�2022-Feb�hX Plant pathogens often adapt to plant genetic resistance so characterization of the architecture underlying such an adaptation is required to understand the adaptive potential of pathogen populations. Erosion of banana quantitative resistance to a major leaf disease caused by polygenic adaptation of the causal agent, the fungus Pseudocercospora fijiensis, was recently identified in the northern Caribbean region. Genome scan and quantitative genetics approaches were combined to investigate the adaptive architecture underlying this adaptation. Thirty-two genomic regions showing host selection footprints were identified by pool sequencing of isolates collected from seven plantation pairs of two cultivars with different levels of quantitative resistance. Individual sequencing and phenotyping of isolates from one pair revealed significant and variable levels of correlation between haplotypes in 17 of these regions with a quantitative trait of pathogenicity (the diseased leaf area). The multilocus pattern of haplotypes detected in the 17 regions was found to be highly variable across all the population pairs studied. These results suggest complex adaptive architecture underlying plant pathogen adaptation to quantitative resistance with a polygenic basis, redundancy, and a low level of parallel evolution between pathogen populations. Candidate genes involved in quantitative pathogenicity and host adaptation of P. fijiensis were identified in genomic regions by combining annotation analysis with available biological data.�h�10.1111/mec.16297�h]�(�Acclimatization��Adaptation, Physiological��Musa��Plant Diseases��Plant Leaves�eu}�(h�36522258�h�JGenome-wide association studies in plant pathosystems: success or failure?�h
]�(�Choghag Demirjian��Fabienne Vailleau��Richard Berthom�Fabrice Roux�eh�Trends in plant science�h�2023-Apr�hX� Harnessing natural genetic variation is an established alternative to artificial genetic variation for investigating the molecular dialog between partners in plant pathosystems. Herein, we review the successes of genome-wide association studies (GWAS) in both plants and pathogens. While GWAS in plants confirmed that the genetic architecture of disease resistance is polygenic, dynamic during the infection kinetics, and dependent on the environment, GWAS shortened the time of identification of quantitative trait loci (QTLs) and revealed both complex epistatic networks and a genetic architecture dependent upon the geographical scale. A similar picture emerges from the few GWAS in pathogens. In addition, the ever-increasing number of functionally validated QTLs has revealed new molecular plant defense mechanisms and pathogenicity determinants. Finally, we propose recommendations to better decode the disease triangle.�h�10.1016/j.tplants.2022.11.006�h]�(�Genome-Wide Association Study��Quantitative Trait Loci�� Phenotype��Plant Diseases�eu}�(h�28885177�h�5Quantitative Genetics of Disease Resistance in Wheat.�h
]�(�Vijai Bhadauria��
Lucia Popescu�eh�#Current issues in molecular biology�h�2018�h�Wheat (�h�10.21775/cimb.027.105�h]�(�Chromosome Mapping��Chromosomes, Plant��Crosses, Genetic��Disease Resistance��Fusarium��Genetic Markers��%High-Throughput Nucleotide Sequencing��Host-Pathogen Interactions��
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