Development and validation of KASP markers for a novel powdery mildew resistance gene in wheat using BSR-Seq analysis

Kaur, R.; Tyagi, V.; Dhariwal, R.; Sheikh, I.; Dhaliwal, H. S.; Sivasamy, M.; Sivakumar, T.; Kumar, S.; Ravat, V. K.; Vasistha, N. K.

doi:10.1101/2025.04.12.648525

bioRxiv · 10.1101/2025.04.12.648525

Development and validation of KASP markers for a novel powdery mildew resistance gene in wheat using BSR-Seq analysis

Kaur, R.·Tyagi, V.·Dhariwal, R.·Sheikh, I.·Dhaliwal, H. S.·Sivasamy, M.·Sivakumar, T.·Kumar, S.·Ravat, V. K.·Vasistha, N. K.

View original source ↗Export metadata ↓

Abstract

Wheat powdery mildew occurs as a devastating infection caused by the pathogenic fungi Blumeeria graminis f. sp. tritici (Bgt). The management of disease becomes much more effective when host resistance methods are employed. The WL711-2U/2B line served as the introgressed line to identify genes linked with powdery mildew resistance. This allowed us to look into the potential resistance components in response to powdery mildew infection. The resistance status of the line towards powdery mildew developed from a single dominant gene named PmAT. Bulked segregant RNA-Seq (BSR-Seq) together with previous QTL-Seq SNP markers helped identify strong candidate regions in chromosome arm 2B extending from 531114848 bp to 530235618 bp. The LOD score from this region reached 72.4 with a PVE% of 64.7, thus proving its main role in resistance. The physical position was subsequently locked up, which was different from the previously identified genes on the same chromosome arm in its position, suggesting that it is most likely a new Pm gene. The QTL interval contained five potential genes that we identified during this research. The five candidate genes directs the protein production, which performs functions linked to the pentatricopeptide repeat family as well as B-box-type zinc finger domain, P-loop-containing nucleoside triphosphate hydrolase, and plant peroxidase. HighlightThe identification of a new wheat powdery mildew resistance gene (PmAT) using a combination of BSR-Seq and QTL-Seq analysis, which located five candidate genes specifically on chromosome 2B.

Explore related subjects

genetics Preprint

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Kaur, R., Tyagi, V., Dhariwal, R., Sheikh, I., Dhaliwal, H. S., Sivasamy, M., Sivakumar, T., Kumar, S., Ravat, V. K., Vasistha, N. K.. 2025-04-18. Development and validation of KASP markers for a novel powdery mildew resistance gene in wheat using BSR-Seq analysis. https://doi.org/10.1101/2025.04.12.648525

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗

bioRxiv2026

Temporal control of mitochondrial mutagenesis reveals the fate of mtDNA mutations with age

Mutations in the mitochondrial genome (mtDNA) play a critical role in the aging process and a wide variety of age-related diseases. However, it remains unclear when the mutations that drive physiological decline arise. To answer this question, we generated a new mouse model in which mitochondrial mutagenesis can be confined to a defined window of time. Surprisingly, we found that mutations that arise during the first two months of life are sufficient to drive a wide variety of age-related pathologies, and that the severity of this pathology is broadly regulated by distinct, tissue-specific selective pressures that control the fate of mtDNA mutations with age. Further, we found that selection against deleterious variants can be modulated by manipulation of mitochondrial fusion in vitro and in vivo. These observations raise the possibility that in some tissues, the pace of aging is pre-determined by events that occur early in life and that interventions targeting mitochondrial fusion may be able to slow down or reverse the expansion of these pathogenic variants. These results carry far-reaching implications for strategies aimed at preventing or delaying age-related decline.

genetics↗

bioRxiv2026

Innate immune stress pathway activation underlies heterochromatin dysfunction pathology

Heterochromatin loss disrupts nuclear architecture, gene regulation and repetitive element silencing, and is associated with diverse human diseases. However, mechanisms linking heterochromatin dysfunction to pathological phenotypes remain unclear. Using genetic interaction screening and genomic analyses in C. elegans, we identify secondary activation of the Intracellular Pathogen Response (IPR), an innate immune stress pathway, as a major contributor to heterochromatin mutant phenotypes. Constitutive IPR activation phenocopies slow growth and indirect transcriptional changes observed in these mutants. Depletion of genetic enhancers further increased, whereas suppressor RNAi attenuated IPR activation, with direct heterochromatin targets remaining substantially deregulated. Notably, many suppressors encode active chromatin components, and mild reduction of RNA polymerase II activity ameliorates growth defects in C. elegans HP1 mutants and human HP1-deficient cells. Our findings reveal secondary stress response activation as an important mechanism linking heterochromatin dysfunction to pathology and identify transcriptional dampening as a potential therapeutic strategy for mitigating these effects.

genetics↗