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Arabidopsis spliceosome factor SmD3-b modulates immunity to Pseudomonas syringae infection

ABSTRACT: Arabidopsis spliceosome factor SmD3-b modulates immunity to Pseudomonas syringae infection

PROVIDER: PRJNA481007 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7518770_1.fastq.gz	Fastqsanger.gz
	SRR7518770_2.fastq.gz	Fastqsanger.gz
	SRR7518771_1.fastq.gz	Fastqsanger.gz
	SRR7518771_2.fastq.gz	Fastqsanger.gz
	SRR7518772_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Arabidopsis spliceosome factor SmD3-b modulates immunity to Pseudomonas syringae infection

Project description:SmD3 is a core protein of small nuclear ribonucleoproteins essential for pre-mRNA splicing. To assess the role of Arabidopsis SmD3-b in response to biotic stress we investigated sensitivity of the smd3-b mutant to Pseudomonas syringae pv. tomato DC3000 infection and its pathogenesis effectors flg22, elf18 and coronatine. We show that the mutant exhibits enhanced susceptibility to Pst accompanied with marked changes in the expression of key pathogenesis markers. mRNA levels of major biotic stress response factors were also altered upon treatment with Pseudomonas effectors. Our genome-wide transcriptome analysis of smd3-b mutant infected with Pst confirmed that lack of SmD3 protein deregulates defense to Pst DC3000 infection on the transcriptional level, including defects in splicing and altered pattern of alternative splicing. In addition, callose deposition, which is another marker of plant immunity, was strongly induced by elf18 and flg22 in the mutant, whereas production of reactive oxygen species triggered by flg22 was reduced. Finally, detection of phosphorylated forms of MPK3, MPK6 and MPK4/11 revealed higher activation of all MAPKs in the smd3-b mutant. All our data indicate that SmD3 contributes to plant immune response possibly via regulation of mRNA splicing of the key pathogenesis factors.

2021-11-17 | GSE117077 | GEO

Arabidopsi s Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection.

Project description:SmD3 is a core component of the small nuclear ribonucleoprotein (snRNP) that is essential for pre-mRNA splicing. The role of Arabidopsis SmD3 in plant immunity was assessed by testing sensitivity of smd3a and smd3b mutants to Pseudomonas syringae pv. tomato (Pst) DC3000 infection and its pathogenesis effectors flagellin (flg22), EF-Tu (elf18) and coronatine (COR). Both smd3 mutants exhibited enhanced susceptibility to Pst accompanied by marked changes in the expression of key pathogenesis markers. mRNA levels of major biotic stress response factors were also altered upon treatment with Pseudomonas effectors. Our genome-wide transcriptome analysis of the smd3b-1 mutant infected with Pst, verified by northern and RT-qPCR, showed that lack of SmD3-b protein deregulates defense against Pst infection at the transcriptional and posttranscriptional levels including defects in splicing and an altered pattern of alternative splicing. Importantly, we show that SmD3-b dysfunction impairs mainly stomatal immunity as a result of defects in stomatal development. We propose that it is the malfunction of the stomata that is the primary cause of an altered mutant response to the pathogen. Other changes in the smd3b-1 mutant involved enhanced elf18- and flg22-induced callose deposition, reduction of flg22-triggered production of early ROS and boost of secondary ROS caused by Pst infection. Together, our data indicate that SmD3 contributes to the plant immune response possibly via regulation of mRNA splicing of key pathogenesis factors.

| S-EPMC8678131 | biostudies-literature

In planta transcriptome analysis of Pseudomonas syringae pv. tomato DC3000 during early infection and early exposure to pattern-triggered immunity in Arabidopsis thaliana

Project description:We develop a protocol for extracting P. syringae transcriptome from infected A. thaliana tissue through physical separation by low speed centrifugation. We use this protocol to compare the RNASeq transcriptome profiles of DC3000 during naïve host infection and exposure to pattern triggered immunity at 1, 3, and 5 hours post inoculation

2018-02-03 | GSE110100 | GEO

Novel JAZ co-operativity and unexpected JA dynamics underpin Arabidopsis defence responses to Pseudomonas syringae infection

Project description:Pathogens target phytohormone signalling pathways to promote disease. Plants deploy salicylic acid (SA) mediated defences against biotrophs. Pathogens antagonise SA immunity by activating jasmonate signalling, e.g. Pseudomonas syringae pv. tomato DC3000 produces coronatine (COR), a jasmonate (JA) mimic. This study found unexpected dynamics between SA, JA and COR and co-operation between JAZ jasmonate repressor proteins during DC3000 infection. JA did not accumulate until late in the infection process and was higher in leaves challenged with coronatine deficient P. syringae or in the more resistant JA receptor mutant coi1. JAZ regulation was complex and coronatine alone was insufficient to sustainably induce JAZs. RNA was extracted from leaves of wild type Col-0 or the jaz5/10 mutant plants from leaves 6, 8, 12 or 16 hours after challenged with Pseudomonas syringae pv. tomato DC3000.

2015-08-28 | E-GEOD-72461 | biostudies-arrayexpress

Novel JAZ co-operativity and unexpected JA dynamics underpin Arabidopsis defence responses to Pseudomonas syringae infection

2015-08-28 | GSE72461 | GEO

Transcriptional responses of wild-type and zin1 mutant Arabidopsis plants to infection with Pseudomonas syringae

Project description:Phytopathogens use secreted effector proteins to suppress host immunity and promote pathogen virulence, and there is increasing evidence that the host-pathogen interactome comprises a complex network. In an effort to identify novel interactors of the Pseudomonas syringae effector HopZ1a, we performed a yeast two-hybrid screen that identified a previously uncharacterized Arabidopsis protein that we designate HopZ1a Interactor 1 (ZIN1). Additional analyses in yeast and in planta revealed that ZIN1 also interacts with several other P. syringae effectors. We show that an Arabidopsis loss-of-function zin1 mutant is less susceptible to infection by certain strains of P. syringae, while overexpression of ZIN1 results in enhanced susceptibility. Functionally, ZIN1 exhibits topoisomerase-like activity in vitro. Transcriptional profiling of wild-type and zin1 Arabidopsis plants inoculated with P. syringae indicated that ZIN1 regulates a wide range of pathogen-responsive biological processes, although the list of genes more highly expressed in zin1 versus wild-type plants was particularly enriched for ribosomal protein genes. Altogether, these data illuminate ZIN1 as a potential susceptibility hub that interacts with multiple effectors to influence the outcome of plant-microbe interactions.

2020-12-09 | GSE158780 | GEO

Transcriptional responses of wild-type and abr1 mutant Arabidopsis plants to infection with Pseudomonas syringae

Project description:Pathogens secrete effector proteins into host cells in order to suppress host immunity and promote pathogen virulence, although many features at the molecular interface of host-pathogen interactions remain to be characterized. In a yeast two-hybrid assay, we found that the Pseudomonas syringae effector HopZ1a interacts with the Arabidopsis transcriptional regulator Abscisic Acid Repressor 1 (ABR1). Further analysis revealed that ABR1 interacts with multiple P. syringae effectors, suggesting that it may be targeted as a susceptibility hub. Indeed, loss-of-function abr1 mutants exhibit reduced susceptibility to a number of P. syringae strains. The ABR1 protein comprises a conserved APETALA2 (AP2) domain flanked by long regions of predicted structural disorder. We verified the DNA-binding activity of the AP2 domain and demonstrated that the disordered domains act redundantly to enhance DNA binding and to facilitate transcriptional activation by ABR1. Finally, we compared gene expression profiles from wild-type and abr1 plants following inoculation with P. syringae, which suggested that the reduced susceptibility of abr1 mutants is due to the loss of a virulence target rather than an enhanced immune response. These data highlight ABR1 as a functionally important component at the host-pathogen interface.

2020-11-24 | GSE153612 | GEO

Spliceosome iCLIP

Project description:Spliceosome iCLIP

| PRJEB27592 | ENA

Transcriptional dynamics driving MAMP-triggered immunity and pathogen effector-mediated immunosuppression in Arabidopsis leaves following infection with Pseudomonas syringae pv. tomato DC3000.

Project description:High-resolution temporal transcriptomic analysis of Arabidopsis thaliana leaves during infection by Pseudomonas syringae DC3000 and DC3000hrpA-thaliana

2015-06-02 | GSE56094 | GEO

The spliceosome factor USP39 promotes hepatocellular carcinoma malignancy through regulating mRNA splicing

Project description:Abnormal alternative splicing (AS) caused by alterations to splicing factors contributes to tumor progression. Nonetheless, the relevant targets and mechanisms remain elusive in hepatocellular carcinoma (HCC). Here, we reported that overexpression of Ubiquitin-specific protease 39 (USP39), a spliceosome component of the U4/U6.U5 tri-snRNP complex, is associated with poor clinical outcomes and proliferative signaling. Functionally, hepatocyte-specific USP39 knockin mice exhibited enhanced hepatocarcinogenesis. In vitro, USP39 promoted HCC cell proliferation and cell cycle progression in a spliceosome-dependent manner. Transcriptomic analysis revealed that USP39 depletion led to comprehensively impaired constitutive splicing and intriguingly, selective AS of hundreds of genes. USP39-mediated splicing switch of KANK2-S to KANK2-L increased the tumorigenic potential of HCC cells through accelerating KANK2 translation. Mechanistically, USP39 modulates exon inclusion/exclusion via interaction with SRSF6 or hnRNPC in a position-dependent manner. These findings highlight a role for USP39 as a splicing regulator in HCC biology and establishing its position-dependent splicing model.

2023-10-24 | PXD035928 | Pride

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