Identificaton of Quantitative Trait Loci Associated with Powdery Mildew and Pepper Mottle Virus Resistance in Pepper

Abstract

Leveillula taurica, the causative agent of powdery mildew disease, and pepper mottle virus (PepMoV) are major pathogens of Capsicum annuum L. They cause damage to the foliage, leading to fruit quality reduction due to sunlight exposure of the fruits, stunted plant growth, reduced yields, and diminished economic returns in severe cases. This research aimed to identify quantitative trait loci (QTL) associated with disease resistance and develop powdery mildew and PepMoV resistant germplasm by evaluating an F2 population derived from a cross between the Serrano pepper ‘Hidalgo’ and the bell pepper ‘Bell 365’. Artificial inoculations and screening for powdery mildew was performed on 151 plants from the original F2 population. A second clonal population consisting of 150 individuals was obtained from the original F2 population and was used for artificial inoculation and screening for PepMoV. Phenotyping of the individuals was performed visually using newly designed symptom description scales as a reference. A double antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) test was used for the PepMoV experiment to confirm the presence of PepMoV in the population. Genotyping-by-sequencing was performed on DNA extracts from the parents and progeny to discover single nucleotide polymorphisms (SNPs). A total of 1078 SNP markers were carefully inspected, and 597 markers were selected and used for genetic map construction and QTL analysis. The genetic map covered 1517.4 cM in total length with an average space of 2.6 cM between markers. A total of 37 highly and 67 moderately resistant individuals to powdery mildew were identified; likewise, PepMoV screening identified 30 resistant plants. Chi-square goodness of fit test and QTL analysis suggested that powdery mildew resistance might be controlled by a single dominant gene located at 31 cM on chromosome 1 responsible for ~49% of the phenotypic variance. Resistance to PepMoV appears to be controlled by a recessive gene located at 4.0 cM on chromosome 6, explaining ~19% of the phenotypic variance.