Publications by authors named "Kav N"

The role of primary metabolism during Brassica napus-Plasmodiophora brassicae interaction leading to clubroot resistance has not yet been investigated thoroughly. In this study, we investigated some of the primary metabolites and their derivatives as well as expression of the genes involved in their biosynthesis to decipher this host-pathogen interaction. For this, two sets (clubroot resistant and susceptible) of canola lines were inoculated with P.

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Clubroot is a destructive root disease of canola ( L.) caused by Woronin. Despite extensive research into the molecular responses of to , there is limited information on proteome- and metabolome-level changes in response to the pathogen, especially during the initial stages of infection.

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Clubroot disease, caused by Plasmodiophora brassicae Woronin, results in severe yield losses in Brassica crops, including canola. Silicon (Si) mitigates several stresses and enhances plant resistance to phytopathogens. We investigated the effects of Si on clubroot disease symptoms in canola at two concentrations of Si, Si: soil in 1: 100 w/w (Si1.

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C2H2-zinc finger (C2H2-ZF) genes are involved in various biological processes in plants including stress response; however, they lack characterization in . We identified 267 C2H2-ZF genes in and deciphered their physiological properties, subcellular localization, structure, synteny, and phylogeny and investigated the expression of 20 genes in response to different stresses and phytohormone treatments. The 267 genes were distributed on 19 chromosomes; phylogenetic analysis categorized them into five clades.

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Clubroot, a devastating soil-borne root disease, in is caused by Woronin ( W.), an obligate biotrophic protist. Plant growth and development, as well as seed yield of crops, are severely affected due to this disease.

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Background: Biotin carboxyl carrier protein (BCCP) is a subunit of Acetyl CoA-carboxylase (ACCase) which catalyzes the conversion of acetyl-CoA to malonyl-CoA in a committed step during the de novo biosynthesis of fatty acids. Lipids, lipid metabolites, lipid-metabolizing and -modifying enzymes are known to play a role in biotic and abiotic stress tolerance in plants. In this regard, an understanding of the Brassica napus BCCP genes will aid in the improvement of biotic and abiotic stress tolerance in canola.

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Clubroot disease caused by Plasmodiophora brassicae is one of the serious threats to canola (Brassica napus L. subsp. napus) production.

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Clubroot of , an economically important soil borne disease, is caused by Woronin, an obligate, biotrophic protist. This disease poses a serious threat to canola and related crops in Canada and around the globe causing significant losses. The pathogen is continuously evolving and new pathotypes are emerging, which necessitates the development of novel resistant canola cultivars to manage the disease.

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Clubroot resistance in spring canola has been introgressed from different Brassica sources; however, molecular mechanism underlying this resistance, especially the involvement of long non-coding RNAs (lncRNAs), is yet to be understood. We identified 464 differentially expressed (DE) lncRNAs from the roots of clubroot-resistant canola, carrying resistance on chromosome BnaA03, and susceptible canola lines challenged with pathotype 3. Pathway enrichment analysis showed that most of the target genes regulated by these DE lncRNAs belonged to plant-pathogen interaction and hormone signaling, as well as primary and secondary metabolic pathways.

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Sclerotinia sclerotiorum is a model necrotrophic pathogen causing great economic losses worldwide. Sclerotia are dormant structures that play significant biological and ecological roles in the life and disease cycles of S. sclerotiorum and other species of sclerotia-forming fungi.

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Food security is affected by climate change, population growth, as well as abiotic and biotic stresses. Conventional and molecular marker assisted breeding and genetic engineering techniques have been employed extensively for improving resistance to biotic stress in crop plants. Advances in next-generation sequencing technologies have permitted the exploration and identification of parts of the genome that extend beyond the regions with protein coding potential.

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Phoma macdonaldii causes black stem of sunflower, which severely affects sunflower yield and quality. There is currently little molecular information available for this pathogenic fungus. In this study, a global proteomic analysis of P.

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Salicylic acid (SA) and reactive oxygen species (ROS) are two well-defined inducers of leaf senescence. Here, we identified a novel WRKY transcription factor gene () in (rapeseed) in promoting SA and ROS production, which eventually led to leaf senescence thereafter. Its expression increased in senescing leaves.

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Gene expression profiles are increasingly applied to investigate molecular mechanism for which, normalization with suitable reference genes is critical. Previously we have reported several suitable reference genes for laticifer samples from rubber tree, however, little is known in leaf. The main objective of this current study was to identify some stable expression reference genes at various developmental stages of leaf, as well as during abiotic (high and low temperature extremes) and biotic stresses (pathogen stress).

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Clubroot disease, caused by Woronin, is a major threat to the production of crops. Resistance to different pathotypes has been reported in the A genome, chromosome A08; however, the molecular mechanism of this resistance, especially the involvement of long noncoding RNAs (lncRNAs), is not understood. We have used a strand-specific lncRNA-Seq approach to catalog lncRNAs from the roots of clubroot-susceptible and -resistant lines.

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Temperature extremes, including cold, adversely impact plant growth and development. Plant responses to cold stress (CS) are regulated at both transcriptional and post-transcriptional levels. MicroRNAs (miRNAs), small non-coding RNAs, are known to be involved in post-transcriptional regulation of various developmental processes and metal stress in Brassica napus L.

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Low temperature is one of the most common environmental stresses that seriously affect the growth and development of plants. However, plants have the plasticity in their defence mechanisms enabling them to tolerate and, sometimes, even survive adverse environmental conditions. MicroRNAs (miRNAs) are small non-coding RNAs, approximately 18-24 nucleotides in length, and are being increasingly recognized as regulators of gene expression at the post-transcriptional level and have the ability to influence a broad range of biological processes.

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Sclerotinia stem rot caused by Sclerotinia sclerotiorum affects canola production worldwide. Emerging evidence suggests that long non-coding RNAs (lncRNAs) play important roles in the regulation of gene expression in plants, in response to both abiotic and biotic stress. So far, identification of lncRNAs has been limited to a few model plant species, and their roles in mediating responses to biotic stresses are yet to be characterized in Brassica napus.

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The necrotrophic phytopathogen, Sclerotinia sclerotiorum, causes Sclerotinia stem rot, which is a serious constraint to canola (Brassica napus L.) production worldwide. To understand the detailed molecular mechanisms underlying host response to Sclerotinia infection, we analyzed the transcript level changes in canola post-infection with S.

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Prions, the causative agent of chronic wasting disease (CWD) enter the environment through shedding of bodily fluids and carcass decay, posing a disease risk as a result of their environmental persistence. Plants have the ability to take up large organic particles, including whole proteins, and microbes. This study used wheat (Triticum aestivum L.

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Canola (oilseed rape, Brassica napus L.) is susceptible to infection by the biotrophic protist Plasmodiophora brassicae, the causal agent of clubroot. To understand the roles of microRNAs (miRNAs) during the post-transcriptional regulation of disease initiation and progression, we have characterized the changes in miRNA expression profiles in canola roots during clubroot disease development and have compared these to uninfected roots.

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Article Synopsis
  • Prion protein (PrP(C)) transitions into an infectious isoform (PrP(Sc)), contributing to severe neurodegenerative diseases called transmissible spongiform encephalopathies.
  • Tricyclic phenothiazine compounds like promazine and chlorpromazine show potential in inhibiting PrP(Sc) formation, but the exact molecular workings are not fully understood.
  • Research indicates that promazine binding induces structural changes in the prion protein and stabilizes certain regions, which may help the normal isoform resist forming harmful aggregates.
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Prion infections cause lethal neurodegeneration. This process requires the cellular prion protein (PrP(C); ref. 1), which contains a globular domain hinged to a long amino-proximal flexible tail.

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Prion diseases are progressive, infectious neurodegenerative disorders caused primarily by the misfolding of the cellular prion protein (PrP(c)) into an insoluble, protease-resistant, aggregated isoform termed PrP(sc). In native conditions, PrP(c) has a structured C-terminal domain and a highly flexible N-terminal domain. A part of this N-terminal domain consists of 4-5 repeats of an unusual glycine-rich, eight amino acids long peptide known as the octapeptide repeat (OR) domain.

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Prion diseases are neurodegenerative diseases characterized by the conversion of the cellular prion protein PrP(c) into a pathogenic isoform PrP(sc). Passive immunization with antiprion monoclonal antibodies can arrest the progression of prion diseases. Here, the crystal structure of the Fab fragment of an antiprion monoclonal antibody, POM1, in complex with human prion protein (huPrP(c)) has been determined to 2.

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