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Ralstonia solanacearum

ABSTRACT: Genome sequencing and analysis of Ralstonia solanacearum phylotype I strains FJAT-91, FJAT-452 and FJAT-462 isolated from tomato, eggplant, and chilli pepper in China

PROVIDER: PRJNA347535 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR4428740_1.fastq.gz	Fastqsanger.gz
	SRR4428740_2.fastq.gz	Fastqsanger.gz
	SRR4431158_1.fastq.gz	Fastqsanger.gz
	SRR4431158_2.fastq.gz	Fastqsanger.gz

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Comparative genomic hybridization by array of several Ralstonia solanacearum strains

Project description:Comparison of the gene content of several Ralstonia solanacearum strains, mainly belonging o the phylotype II; according to this pangenomic microarray, genes were deemed present or absent

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Ralstonia solanacearum FJAT-91

Project description:Ralstonia solanacearum virulent strain FJAT-91 Genome Sequencing

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Ralstonia solanacearum FJAT-91

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Impact of pehR transcriptional regulator on Ralstonia solanacearum F1C1 gene expression patterns

Project description:Ralstonia solanacearum, recognized as a pervasive plant pathogen causing lethal wilt disease in over 450 plant species worldwide, represents a substantial threat to economically vital crops including tomato, chili, and eggplant. Within R. solanacearum, pehR serves as a transcriptional regulator, forming part of the pehSR two-component regulatory system. This system governs the production of polygalacturonase (PG), a crucial extracellular enzyme involved in plant cell wall degradation and bacterial wilt development. Our study focuses on a disruption mutant of the pehR gene from the local isolate R. solanacearum F1C1, obtained from Tezpur, Assam. Utilizing RNA-seq, we examine the gene expression profiles of R. solanacearum F1C1 under pehR regulation. Differential expression analysis between wild type and pehR mutants reveals a set of genes directly influenced by pehR. This comprehensive gene expression analysis provides insights into the system-level responses orchestrated by the pehR regulator in pathogenicity and virulence development. Moreover, it sheds light on the broader regulatory network controlled by pehR and its underlying molecular mechanisms. Our work also underscores the identification of key target genes regulated by pehR within R. solanacearum F1C1, offering a deeper understanding of its role in bacterial pathogenicity. Ultimately, unraveling the complete pehR regulome holds promise for elucidating the regulatory dynamics driving the pathogenic behavior of R. solanacearum F1C1.

2024-11-22 | GSE269108 | GEO

Ralstonia solanacearum FJAT-1458

Project description:The complete genome sequence of Ralstonia solanacearum FJAT-1458

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Ralstonia solanacearum FJAT-1458

Project description:Whole genome sequencing of R. solanacearum avirulent strain FJAT-1458

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Expression data in response to pepper leaf curl virus (PepLCV) infection in Chilli pepper at three leaf stage

Project description:A comparative study to determine the pepper leaf curl virus resistance machanism between resistant and susceptible genotypes at three leaf stage. To study the molecular mechanism of pepper leaf curl virus (PepLCV) resistance, pepper plants were exposed to PepLCV through artificial inoculation and hybridization on Agilent tomato microarrays. The expression analysis of PepLCV resistant and susceptible genotypes after artificial inoculation at three leaf stage showed that the resistance against PepLCV is due to sum of expression of hundreds of genes at a particular stage. Tomato microarrays consisting of 43,803 probes were used for whole genome expression analysis of chilli peppers for resistance against PepLCV. Transcripts from the leaves of resistant (BS-35) and susceptible plants (IVPBC-535) were compared in response to PepLCV inoculation at three leaf stage.

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Gene expression analysis of Mulberry root after inoculation with Ralstonia solanacearum.

Project description:Bacterial wilt, caused by the soil-borne bacterium Ralstonia solanacearum, is a lethal disease of mulberry, but the molecular mechanisms of the host resistance responses to R. solanacearum remain unclear. In order to better understand molecular resistance mechanisms to R. solanacearum in mulberry, we set out to define the changes in gene expression of resistance and susceptible mulberry cultivars after inoculation with R. solanacearum. Susceptible cultivar YSD10, resistance cultivar KQ10 and YS283 were inoculation with R. solanacearum, mulberry root samples were collected at 1 dpi and non-treated control in all cultivars. Then we performed RNA-Seq analyses on all mulberry root samples using Illumina HiSeq 2000.

2019-06-13 | GSE60030 | GEO

RNA-seq analysis of Ralstonia solanacearum treated with nitrosative and oxidative stress

Project description:Ralstonia solancearum causes bacterial wilt disease on diverse plant hosts. R. solanacearum cells enter a host from soil or infested water through the roots, then multiply and spread in the water-transporting xylem vessels. Despite the low nutrient content of xylem sap, R. solanacearum grows extremely well inside the host, using denitrification to respire in this hypoxic environment. R. solanacearum growth in planta also depends on the successful deployment of protein effectors into host cells using a Type III Secretion System (T3SS). The T3SS is absolutely required for R. solanacearum virulence, but it is metabolically costly and can trigger host defenses. Thus, the pathogen’s success depends on optimized regulation of the T3SS. We found that a byproduct of denitrification, the toxic free-radical nitric oxide (NO), positively regulates the R. solanacearum T3SS both in vitro and in planta. Using chemical treatments and R. solanacearum mutants with altered NO levels, we show that the expression of a key T3SS regulator is induced by NO in culture. Analyzing the transcriptome of R. solanacearum responding to varying levels of NO both in culture and in planta revealed that the T3SS and effectors were broadly upregulated with increasing levels of NO. This regulation was specific to the T3SS and was not shared by other stressors. Our results suggest that R. solanacearum experiences an NO-rich environment in the plant host and may use this NO as a signal to activate T3SS during infection.

2020-10-26 | GSE160024 | GEO