Pfcyp51 exclusively determines reduced sensitivity to 14α-demethylase inhibitor fungicides in the banana black Sigatoka pathogen Pseudocercospora fijiensis

Autor: Pablo Chong, Aikaterini Eleni Vichou, Rafael Arango Isaza, Harold J. G. Meijer, Gert H. J. Kema, Henk J. Schouten
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Leaves
Black sigatoka
Heredity
Genetic Linkage
Physical Mapping
Plant Science
Bananas
Gene mutation
Genetic analysis
Sterol 14-Demethylase
Promoter Regions
Genetic
Fungicides
Genetics
education.field_of_study
Multidisciplinary
Plant Anatomy
Fungal genetics
Eukaryota
Agriculture
Plants
14-alpha Demethylase Inhibitors
Medicine
Agrochemicals
PBR Biodiversity and genetic variation
Research Article
Science
Population
Mycology
Biology
Research and Analysis Methods
Fruits
Fungal Proteins
Biointeractions and Plant Health
PBR Biodiversiteit en Genetische Variatie
Gene mapping
Ascomycota
Drug Resistance
Fungal
Life Science
Fungal Genetics
education
Molecular Biology Techniques
Linkage Mapping
Gene
Molecular Biology
Plant Diseases
Gene Mapping
Organisms
Biology and Life Sciences
Musa
Laboratorium voor Phytopathologie
Fungicides
Industrial
Plant Leaves
Plant Breeding
Genetic marker
Laboratory of Phytopathology
Mutation
EPS
human activities
Zdroj: PLoS ONE, Vol 14, Iss 10, p e0223858 (2019)
PLoS ONE
PLoS ONE 14 (2019) 10
PLoS ONE, 14(10)
ISSN: 1932-6203
Popis: The haploid fungus Pseudocercospora fijiensis causes black Sigatoka in banana and is chiefly controlled by extensive fungicide applications, threatening occupational health and the environment. The 14α-Demethylase Inhibitors (DMIs) are important disease control fungicides, but they lose sensitivity in a rather gradual fashion, suggesting an underlying polygenic genetic mechanism. In spite of this, evidence found thus far suggests that P. fijiensis cyp51 gene mutations are the main responsible factor for sensitivity loss in the field. To better understand the mechanisms involved in DMI resistance, in this study we constructed a genetic map using DArTseq markers on two F1 populations generated by crossing two different DMI resistant strains with a sensitive strain. Analysis of the inheritance of DMI resistance in the F1 populations revealed two major and discrete DMI-sensitivity groups. This is an indicative of a single major responsible gene. Using the DMI-sensitivity scorings of both F1 populations and the generation of genetic linkage maps, the sensitivity causal factor was located in a single genetic region. Full agreement was found for genetic markers in either population, underlining the robustness of the approach. The two maps indicated a similar genetic region where the Pfcyp51 gene is found. Sequence analyses of the Pfcyp51 gene of the F1 populations also revealed a matching bimodal distribution with the DMI resistant. Amino acid substitutions in P. fijiensis CYP51 enzyme of the resistant progeny were previously correlated with the loss of DMI sensitivity. In addition, the resistant progeny inherited a Pfcyp51 gene promoter insertion, composed of a repeat element with a palindromic core, also previously correlated with increased gene expression. This genetic approach confirms that Pfcyp51 is the single explanatory gene for reduced sensitivity to DMI fungicides in the analysed P. fijiensis strains. Our study is the first genetic analysis to map the underlying genetic factors for reduced DMI efficacy.
Databáze: OpenAIRE
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