Search bioRxiv⌕ Search

Biology subjects

Kumari, H.

Publications and source records attributed to Kumari, H..

2 recordsLinked to original sources
bioRxiv2026

Apple scar skin viroid disease induced physicochemical and metabolic alterations in Apples

Apple scar skin disease (ASSD), caused by Apple scar skin viroid (ASSVd), is characterized by peel scarring, cracking, dappling, and fruit deformation, resulting in reduced fruit quality and marketability. Despite its economic importance, the physicochemical and metabolic alterations underlying disease progression remain poorly understood. To address this knowledge gap, apple fruits representing four stages of ASSD (healthy, lightly infected, moderately infected, and highly infected) were comprehensively characterized. ASSVd infection was confirmed by RT-PCR, amplicon sequencing, and phylogenetic analysis. Fruit morphology and quality attributes, including firmness, total soluble solids (TSS), pH, titratable acidity (TA), and total phenolic content (TPC), were evaluated. ASSVd infection significantly reduced fruit weight and firmness and altered TSS and TA, indicating progressive deterioration of fruit quality. To investigate the underlying metabolic changes, peel and pulp tissues were analysed separately using gas chromatography-mass spectrometry (GC-MS), while major soluble sugars were quantified by 1H nuclear magnetic resonance (1H NMR) spectroscopy. Integrated metabolomic analyses revealed distinct tissue-specific metabolic reprogramming during disease progression. Major soluble sugars declined significantly during early infection, followed by tissue-dependent recovery at later stages, whereas organic acids, amino acids, phenolics, lipids, polyols, and pentacyclic triterpenoids exhibited dynamic stage-dependent changes. Notably, lupeol accumulated progressively, whereas ursolic acid and oleanolic acid declined, indicating disease-associated alterations in host triterpenoid metabolism. Multivariate analyses demonstrated clear metabolic separation among disease stages. Lupeol, ursolic acid, and chlorogenic acid were identified as candidate discriminatory metabolites in the peel, whereas myo-inositol, chlorogenic acid, and aspartic acid were identified in the pulp. Collectively, these findings demonstrate that ASSD induces coordinated, tissue-specific physicochemical and metabolic reprogramming that compromises postharvest fruit quality and reshapes defence-associated metabolism. This study provides the first integrated metabolomic characterization of ASSD progression and identifies potential metabolic biomarkers for disease diagnosis and severity assessment. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=142 SRC="FIGDIR/small/741181v1_ufig1.gif" ALT="Figure 1"> View larger version (56K): org.highwire.dtl.DTLVardef@50763eorg.highwire.dtl.DTLVardef@82eaddorg.highwire.dtl.DTLVardef@1096b06org.highwire.dtl.DTLVardef@15161b4_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗
bioRxiv2018

Alginate-regulating genes are identified in the clinical cystic fibrosis isolate of Pseudomonas aeruginosa PA2192

Cystic fibrosis (CF) is a genetic disorder that leads to a buildup of mucus in the lungs ideal for bacterial colonization. When Pseudomonas aeruginosa enters the CF lung, it undergoes a conversion from nonmucoid to mucoid; colonization by a mucoid strain of P. aeruginosa greatly increases mortality. The mucoid phenotype is due to the production of alginate. The regulator of alginate production is the AlgT/U sigma factor. The observed phenotypic conversion is due to a mutation in the mucA gene coding for an anti-sigma factor, MucA, which sequesters AlgT/U. This mucoid phenotype is unstable when the strains are removed from the lung as they acquire second-site mutations. This in vitro reversion phenomenon is utilized to identify novel genes regulating alginate production. Previously, second-site mutations were mapped to algT/U, algO, and mucP, demonstrating their role in alginate regulation. Most of these studies were performed using a non-CF isolate. It was hypothesized that second site mutations in a clinical strain would be mapped to the same genes. In this study, a clinical, hyper-mucoid P. aeruginosa strain PA2192 was used to study the reversion phenomenon. This study found that PA2192 has a novel mucA mutation which was named them mucA180 allele. Twelve colonies were sub-cultured for two weeks without aeration at room temperature in order to obtain nonmucoid suppressors of alginate production (sap). Only 41 sap mutants were stable for more than 48 hours -- a reversion frequency of 3.9% as compared to ~90% in laboratory strains showing that PA2192 has a stable mucoid phenotype. This phenotype was restored in 28 of the 41 sap mutants when complemented with plasmids harboring algT/U. Four of the sap mutants are complemented by algO. Sequence analyses of the algT/U mutants have found no mutations in the coding region or promoter leading to the hypothesis that there is another, as yet unidentified mechanism of alginate regulation in this clinical strain.

microbiology↗