These findings establish qPB10 as the primary locus governing Phytophthora blight resistance in sesame, and kompetitive allele-specific PCR (KASP) markers were developed based on sequence polymorphisms within the qPB10 interval that reliably discriminates resistant genotypes.
Abstract
Background
Phytophthora blight, caused by Phytophthora nicotianae, is a destructive disease that severely affects sesame (Sesamum indicum L.). Developing resistant cultivars remains the most effective management strategy. This study aimed to identify genomic regions associated with Phytophthora blight resistance and to develop molecular markers for use in sesame breeding.
Results
Whole-genome resequencing (WGS) was performed for the resistant cultivar Geonbaek, the susceptible cultivar Milsung, and 99 recombinant inbred lines (RILs). Using a high-density genetic map, we identified a major resistance locus on chromosome 10, designated qPB10. The IM-ADD analysis defined a 0.51-Mb marker interval with an LOD score of 25.67, and a complementary binary-trait analysis independently detected the same locus at 75.10 cM. Genomic analysis of the target region revealed several immune-related genes, including clusters encoding nucleotide-binding leucine-rich repeat (NLR) proteins and other defense-associated factors. To utilize these findings in breeding, kompetitive allele-specific PCR (KASP) markers were developed based on sequence polymorphisms within the qPB10 interval. Validation using the RIL population and a diverse panel of sesame cultivars identified a robust marker that reliably discriminates resistant genotypes.
Conclusion
These findings establish qPB10 as the primary locus governing Phytophthora blight resistance in sesame. The KASP markers developed in this study enable efficient marker-assisted selection without the need for extensive disease phenotyping. These results provide a practical genomic resource for accelerated breeding of resistant cultivars and establish a foundation for future functional characterization of resistance mechanisms.
Phytophthora capsici
is a destructive pathogen of pepper (
Capsicum annuum
L.), causing severe yield losses worldwide. Although resistance loci derived from the
C. annuum
landrace CM334 have been widely deployed, durable resistance remains elusive due to complex inheritance and the reported
Inhibitor of P. capsici resistance
(
Ipcr
) gene that suppresses resistance. We investigated the inheritance and genomic location of
Ipcr
using an F
2
population derived from a hybridization between CM334 and NMCA10399. Disease evaluations with a virulent
P. capsici
isolate revealed segregation did not deviate from a 3:13 ratio, consistent with dominant suppression epistasis. Bulk segregant analysis with quantitative trait loci sequencing identified a major susceptibility-associated interval on chromosome 3 (107.6 to 113.4 Mb) significantly associated with susceptibility, in which ΔSNP index values reached –0.62 and G′ statistics exceeded significance thresholds, consistent with dominant suppression of resistance. Candidate gene analysis within this region revealed loci with potential roles in defense regulation, including a CLAVATA3/ESR-related protein, calmodulin-binding protein 60, ASC1-like protein, MLO-like gene, and PBS1-like kinase. These findings refine the genomic position of
Ipcr
and highlight candidate genes that may condition susceptibility, providing valuable targets for functional validation and breeding strategies to eliminate suppressive alleles and develop durable resistance to
P. capsici
in pepper.
Unknown authors· J. Amer. Soc. Hort. Sci.· 0 citations
Maize, as a globally important food crop, is threatened by pests including the fall armyworm (FAW, Spodoptera frugiperda) throughout its production. Current management strategies are largely limited to conventional chemical insecticides and transgenic maize varieties. However, the identification and functional characterization of endogenous insect-resistance genes within maize inbred line populations, as well as the underlying molecular mechanisms governing resistance, remain poorly understood. Here, we systematically evaluate FAW resistance on 300 modern maize inbred lines and 200 recombinant inbred lines (RIL) populations in field, followed by quantitative trait locus (QTL) and genome-wide association studies (GWAS) mapping to screen candidate genes. Our data demonstrate that a β-glucosidase ZmBGLU17 was identified as a key FAW resistance gene, which contributes to the accumulation of two defense metabolites, lignin and DIMBOA. Overexpression of the ZmBGLU17 gene confers enhanced resistance to the FAW by significantly reducing larval survival. Haplotype analysis revealed two distinct haplotypes, with haplotype 1 demonstrating significantly enhanced resistance to FAW infestation compared with haplotype 2. Jointly, our research identified ZmBGLU17 as a key resistance-associated gene against FAW and confirmed its functional role through rigorous genetic validation. Furthermore, haplotype analysis revealed prevalent resistance-linked haplotypes, thereby establishing a molecular foundation for the development of FAW-resistant maize inbred lines.
Net form net blotch (NFNB), caused by
Pyrenophora teres
f.
teres
(
Ptt
), is a major constraint to barley production. However, the genetic basis of adult plant resistance (APR) and seedling resistance remains incompletely understood. This study aimed to dissect the genetic architecture of NFNB resistance in a diverse panel of 273 spring barley accessions.
APR was evaluated in two contrasting field environments in Kazakhstan, whereas seedling resistance was assessed under greenhouse conditions using two
Ptt
races. Genotyping with the 50K SNP array yielded 31,834 high-quality SNPs. Genome-wide association analyses were performed using four models – MLM, MLMM, FarmCPU, and BLINK – that accounted for population structure and kinship. Candidate genes within QTL intervals were prioritized using transcriptomic data from 16 barley tissues and co-expression network analysis.
Substantial phenotypic variation was observed, with moderate heritability for APR (
h
2
= 50.6%) and seedling resistance (
h
2
= 41.3%), together with strong genotype × environment and genotype × race interactions. In total, 275 marker–trait associations were detected for APR and 48 for seedling resistance. These associations were consolidated into 57 genome-wide significant (P < 1.57E–6) or multi-model-supported QTLs across all seven barley chromosomes, including 39 APR and 18 seedling-resistance QTLs. Forty QTLs co-localized with known resistance genes (
Rpt1
,
Rpt2
,
Rpt3
,
Rpt4
,
Rpt6
,
Rpt8
,
Rpt9
, and
SPN1
) or previously reported net blotch QTLs, whereas 17 were potentially novel. Transcriptomic integration identified 87 highly expressed genes within APR QTL regions and 42 within seedling-resistance QTLs. The potentially novel QTLs
Q_NB_1H.6
,
Q_NB_2H.3
, and
Q_NB_3H.1
harbored genes encoding proteins previously associated with pathogen resistance and stress responses. Co-expression analysis revealed stage-specific transcriptional patterns, with APR-associated genes enriched in regulatory functions and seedling-resistance genes enriched in metabolic and structural functions.
The results demonstrate that NFNB resistance is polygenic and developmentally stage-dependent, with partly distinct mechanisms underlying adult plant and seedling resistance. The identified QTLs and prioritized candidate genes provide targets for independent validation, functional characterization, and the development of molecular markers to support breeding for durable NFNB resistance in barley.
Y. Genievskaya, A. Maulenbay, A. Zatybekov et al.· Frontiers in Agronomy· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
