Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1108018 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Arabipdosis thaliana (ecotype Col-0) was infected with the root pathogen Plasmodiophora brassicae. Gene expression of the host plant has been analyzed at two time points after inoculation (10 and 23 days after inoculation) compared to the correspondend control plants.
2005-02-25 | E-MEXP-254 | biostudies-arrayexpress
Project description:Plasmodiophora brassicae transcriptome.
| PRJNA771176 | ENA
Project description:Clubroot (Plasmodiophora brassicae) is a pathogen of Brassicaceae that causes significant reductions in yield as a consequence of gall formation in the root and hypocotyl of infected plants. The pathogen hijacks host vascular cambium development and cytokinins are implicated in this process. RNASeq was used to investigate changes in cytokinin metabolism during gall formation of clubroot-infected Arabidopsis thaliana. RNASeq analysis of infected tissue showed that host cytokinin metabolism was strongly down-regulated both at the onset (16 DPI) and late (26 DPI) stages of gall formation. Expression of host genes associated with cytokinin biosynthesis, signalling, degradation and conjugation was strongly repressed. Two isopentenyltransferase genes associated with cytokinin biosynthesis are present in the P. brassicae genome and are expressed throughout gall formation.
2016-07-04 | E-MTAB-4176 | biostudies-arrayexpress
Project description:Transcriptome study of kohlrabi crops infected with Plasmodiophora brassicae
| PRJEB26435 | ENA
Project description:Although Plasmodiophora brassicae is one of the most common pathogens worldwide, the causal agent of clubroot disease in Brassica crops, resistance mechanisms to it are still only poorly understood. To study the early defense response induced by P. brassicae infection, a global transcriptome profiling of the roots of two near-isogenic lines (NILs) of clubroot-resistant (CR BJN3-2) and clubroot-susceptible (BJN3-2) Chinese cabbage (Brassica rapa) was performed by RNA-seq. Among the 42,730 unique genes mapped to the reference genome of B. rapa, 1,875 and 2,103 genes were found to be up- and down-regulated between CR BJN3-2 and BJN3-2, respectively, at 0, 12, 72, and 96 hours after inoculation (hai). Functional annotation showed that most of the differently expressed genes are involved in metabolism, transport, signal transduction, and defense. Of the genes assigned to plant-pathogen interactions, 151 showed different expression patterns between two NILs, including genes associated with pathogen-associated molecular patterns (PAMPs) and effectors recognition, calcium ion influx, hormone signaling, pathogenesis-related (PR) genes, transcription factors, and cell wall modification. In particular, the expression level of effector receptors (resistance proteins), PR genes involved in salicylic acid (SA) signaling pathway, were higher in clubroot-resistant NIL, while half of the PAMP receptors were suppressed in CR BJN3-2. This suggests that there was a more robust effector-triggered immunity (ETI) response in CR BJN3-2 and that SA signaling was important to clubroot resistance. The dataset generated by our transcriptome profiling may prove invaluable for further exploration of the different responses to P. brassicae between clubroot-resistant and clubroot-susceptible genotypes, and it will strongly contribute to a better understanding of the molecular mechanisms of resistance genes of B. rapa against P. brassicae infection.
2016-02-01 | GSE74044 | GEO
Project description:The clubroot disease caused by the obligate biotrophic protist Plasmodiophora brassicae on host plants of the Brassicaceae family is characterized by enhanced cell division and cell expansion. Since a typical root section of an infected plant always includes different stages of the pathogen as well as uninfected cells, we were interested to investigate specific developmental stages of the pathogen and their effect on host transcriptional changes. We extended previous microarray studies on whole roots by using Laser Microdissection and Pressure Catapulting (LMPC) to isolate individual cells harboring defined developmental stages of the pathogen. In addition, we compared the central cylinder of infected to contol plants. We were especially interested to elucidate the stage-specific hormonal network. The upregulation of genes involved in auxin and cytokinin metabolism and signaling was confirmed. In addition, we found evidence that brassinosteroid (BR) synthesis and signal perception was in many cases upregulated in enlarged cells and the central cylinder. This was confirmed by qPCR and mutant analysis of the BR receptor mutant bri1-6, which exhibited less severe gall formation than the respective wild type. Our results identify novel hormone pathways involved in clubroot development. Using this method of single cell preparation combined with transcriptome analysis has been very useful to elucidate the regulation of gall growth by this obligate biotropic pathogen in a cell- and stage-specific manner. Transcription profiling was performed in isolated Arabidopsis thaliana root cells harboring different developmental stages of Plasmodiophora brassicae at two time points after inoculation (dai) (14 and 21 dai), as well as in infected central cylinder tissue from roots at 14 dai (days after inoculation). Control samples were taken from uninfected roots. Host cells were dissected from paraffin embedded roots using Laser Microdissection and Pressure Catapulting (LMPC). 8 samples have been analyzed.
2014-02-23 | E-GEOD-44676 | biostudies-arrayexpress
Project description:Clubroot (Plasmodiophora brassicae) is a pathogen of Brassicaceae that causes significant reductions in yield as a consequence of gall formation in the root and hypocotyl of infected plants. The pathogen hijacks host vascular cambium development and cytokinins are implicated in this process. Microarray analysis was used to investigate changes in cytokinin metabolism during gall formation of clubroot-infected ipt1;3;5;7 mutants Arabidopsis thaliana. These mutants have severely restricted synthesis of host cytokinins (isopentenyl adenine and trans zeatin) and fail to form a vascular cambium and, as a consequence, do not undergo secondary thickening. Infection of these mutants allows the impact of pathogen-derived cytokinin synthesis to be observed.
2016-01-12 | E-MTAB-4201 | biostudies-arrayexpress
Project description:Gall formation on the belowground parts of plants infected with Plasmodiophora brassicae is the result of extensive host cellular reprogramming. The development of these structures is a consequence of increased cell proliferation followed by massive enlargement of cells colonised with the pathogen. Drastic changes in cellular growth patterns create local deformities in the roots and hypocotyl giving rise to mechanical tensions within the tissue of these organs. Host cell wall extensibility and recomposition accompanies growth of the gall, influences pathogen spread and also pathogen life cycle progression. Demethylation of pectin within the extracellular matrix may play an important role in P. brassicae-driven hypertrophy of host underground organs. Through proteomic analysis of the cell wall we identified proteins accumulating in the galls developing on the underground parts of Arabidopsis thaliana plants infected with P. brassicae. One of the key proteins identified was the pectin methylesterase PME18; we further characterised its expression and conducted functional and anatomic studies in the knock-out mutant and used Raman spectroscopy to study the status of pectin in P. brassicae infected galls. We found that late stages of gall formation are accompanied with increased levels of Pectin Methylesterase 18 (PME18). We have also shown, that the massive enlargement of cells colonised with P. brassicae coincides with decreases in pectin methylation. In pme18-1 knock-out mutants P. brassicae could still induce demethylation; however, the galls in this line were smaller and cellular expansion was less pronounced. Alteration in pectin demethylation in the host resulted in changes in pathogen distribution and slowed down disease progression. To conclude, P. brassicae driven host organ hypertrophy observed during clubroot disease is accompanied by pectin demethylation in the extracellular matrix. The pathogen hijacks endogenous host mechanisms involved in cell wall loosening to create an optimal cellular environment for completion of its life cycle and eventual release of resting spores facilitated by degradation of demethylated pectin polymers.
2021-07-20 | PXD026660 | Pride