RNA-seq data of Phytophthora infestans 88069 infected tomato leaves
Ontology highlight
ABSTRACT:
ORGANISM(S): Solanum lycopersicum
PROVIDER: GSE140537 | GEO | 2022/10/01
REPOSITORIES: GEO
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Project description:The process of RNA splicing influences many physiological processes including plant immunity. However, how plant parasites manipulate host RNA splicing process remains unknown. Here we demonstrate that PsAvr3c, an avirulence effector from oomycete plant pathogen Phytophthora sojae, physically binds to and stabilizes soybean (Glycine max) serine/lysine/arginine rich proteins GmSKRPs in vivo. The SKRPs are novel proteins that associate with spliceosome components, and are negative regulators of plant immunity. Analysis by RNA-seq data indicates that alternative splicing of pre-mRNAs from 401 soybean genes, including defense related genes, is altered in GmSKRP1 and PsAvr3c over-expressing lines compared to control plants. Representative splicing events mediated by GmSKRP1 and PsAvr3c are tested by infection assays or by transient expression in soybean plants. Our results show that a plant pathogen effector can reprogram host pre-mRNA splicing to promote disease, and we propose that pathogens evolved such strategies to defeat host immune systems.
2018-01-12 | GSE100985 | GEO
Project description:Pathogens modulate host cell structure and function by secreting effectors into host tissues. Effectors generally function by associating with host molecules and co-opting or perturbing their activities. This study aimed at identifying the plant proteins associated with the RXLR class of host-translocated effectors of the potato blight pathogen Phytophthora infestans in order to identify the host processes targeted by these effectors. We carried out an in planta screen by transiently expressing P. infestans RXLR effectors in Nicotiana benthamiana leaves followed by co-immunoprecipitation (co-IP) and liquid chromatography tandem mass spectrometry (LC-MS/MS). This generated an effector-host protein interactome matrix of 59 P. infestans RXLR effectors x 586 N. benthamiana proteins. Classification of the host interactors into putative functional categories revealed over 35 biological processes that are candidate effector-targeted pathways. We further characterized the PexRD12/31 family of RXLR-WY effectors, which associate and co-localize with components of vesicle trafficking machinery. One member of this family, PexRD31, increased the number of GFP-2xFYVE labeled vesicles in N. benthamiana cells. We also noted an accumulation of FYVE vesicles in areas of N. benthamiana leaves colonized by P. infestans indicating that this pathogen may enhance endosomal trafficking. We hope that the interactome dataset we generated will serve as a useful community resource for functional studies of P. infestans effectors.
2020-09-23 | PXD020751 | Pride
Project description:Infection by Albugo species, resulting in white rust disease, suppresses host plant immunity, and can even enable Albugo laibachii-infected Arabidopsis to support growth and reproduction of the non-host potato late blight pathogen Phytophthora infestans. However, the mechanisms involved in non-host resistance remain to be elucidated. Here, we investigate specific host defense mechanisms that are suppressed by A. laibachii and A. candida infection, and compare the resistance contributed by indole glucosinolates and camalexin to that resulting from other components of defense induced by salicylic acid. We conclude a broad repertoire of host defense components contributes to non-host resistance in Arabidopsis to P. infestans, with a particular role for tryptophan-derived anti-microbial metabolites. Identifying the mechanisms involved in non-host resistance to pathogens such as P. infestans is necessary in the development of strategies to ensure future food security.
2017-05-08 | GSE75016 | GEO
Project description:One fascinating aspect of plant pathogen co-evolution is that pathogens use effectors to alter a broad range of host responses. RNA splicing functions in many physiological processes including plant immunity. However, how plant pathogens manipulate host RNA splicing process remains unknown. Here we demonstrate that PsAvr3c, an avirulence effector from oomycete pathogen Phytophthora sojae, physically binds to and stabilizes soybean (Glycine max) serine/arginine/lysine rich proteins GmSRKPs in vivo. SRKP, novel proteins associating with spliceosome components, are plant susceptibility factors against Phytophthora. Furthermore, RNA-seq data uncovers that differential splicing over one thousand soybean mRNA transcripts, including defense related genes, are significantly changed in GmSRKP1 over-expressing lines. Representative splicing events are verified in either infection assay or soybean transient expression assay. Our results demonstrate that plant pathogen utilize effector to reprogram host RNA splicing, uncovering a new strategy evolved by pathogens to defeat host immune system
2019-10-20 | GSE88973 | GEO
Project description:To effectively manage resources, regulatory cross-talk between biological processes within an organism is essential. An emerging area in plant research focuses on antagonism between regulatory systems controlling growth/development and those governing immunity. Such crosstalk represents a point of vulnerability for pathogens to exploit. Here we show that the notorious potato blight pathogen Phytophthora infestans promotes a growth and development pathway in order to antagonise plant immunity. AVR2, an effector protein secreted by P. infestans, has been shown to interact with potato BSL1, a putative phosphatase implicated in brassinosteroid hormone signalling. Plants expressing AVR2 exhibit transcriptional and phenotypic overlaps with an over-active brassinosteroid signalling pathway, and have compromised immunity. The activity of AVR2 leads to up-regulation of a functional orthologue of AtHBI1, known to facilitate cross-talk between the brassinosteroid pathway and immune signalling in Arabidopsis. Transient expression of potato HBI1-like compromises immunity and enhances leaf colonisation by P. infestans. Knowledge of how pathogens manipulate regulatory cross-talk governing resource allocation in plants will inform crop breeding efforts of the future; helping to maximise both yield and resistance to ensure food security as pressure on our agricultural systems increases.
2017-03-01 | E-MTAB-3854 | biostudies-arrayexpress
Project description:Pathogens produce diverse effector proteins to manipulate host cellular processes. However, how functional diversity is generated in an effector repertoire is poorly understood. Many effectors in the devastating plant pathogen Phytophthora contain tandem repeats of the “(L)WY” motif, which are structurally conserved but variable in sequences. Here, we discovered a functional module formed by a specific (L)WY-LWY combination in multiple Phytophthora effectors, which efficiently recruit the Serine/Threonine protein phosphatase 2A (PP2A) core enzyme in plant hosts. Crystal structure of an effector-PP2A complex shows that the (L)WY-LWY module enables hijacking of the host PP2A core enzyme to form functional holoenzymes. While sharing the PP2A-interacting module at the amino terminus, these effectors possess divergent C-terminal LWY units and regulate distinct sets of phosphoproteins in the host. Our results highlight the appropriation of an essential host phosphatase through molecular mimicry by pathogens and diversification promoted by protein modularity in an effector repertoire.
2023-06-26 | PXD042330 | Pride
Project description:Pre-mRNA splicing is regulated through combinatorial activity of RNA motifs including splice sites and splicing regulatory elements (SREs). Here, we show that the activity of a major class of mammalian SREs is highly sensitive to the strength of the adjacent 5' splice site (5'ss) sequence, and that this has important functional and evolutionary implications. Activity of G-run SREs was higher for intermediate strength 5'ss by ~4-fold relative to weak 5'ss, and by ~1.3-fold relative to strong 5'ss. The dependence on 5'ss strength was supported both by comparative genomics and by microarray and Illumina mRNA-Seq analyses of splicing changes following RNAi against the splicing factor heterogeneous nuclear ribonucleoprotein (hnRNP) H, which binds G-runs. This dependence implies that the responsiveness of exons to changes in hnRNP H levels is a bivariate function of both SRE abundance and 5'ss strength; this relationship may hold also for other splicing factors. This pattern of activity enables G-runs and hnRNP H to buffer the effects of 5'ss mutations, augmenting both the frequency of 5'ss polymorphism and the evolution of new splicing patterns. Examine mRNA expression in 293T cells following hnRNP H or control siRNA knockdown
2009-09-12 | E-GEOD-16642 | biostudies-arrayexpress
Project description:Alternative mRNA splicing is a major mechanism for gene regulation and transcriptome diversity. Despite the extent of the phenomenon, the regulation and specificity of the splicing machinery are only partially understood. Adenosine-to-inosine (A-to-I) RNA editing of pre-mRNA by ADAR enzymes has been linked to splicing regulation in several cases. Here we used bioinformatics approaches, RNA-seq and exon-specific microarray of ADAR knockdown cells to globally examine how ADAR and its A-to-I RNA editing activity influence alternative mRNA splicing. Although A-to-I RNA editing only rarely targets canonical splicing acceptor, donor, and branch sites, it was found to affect splicing regulatory elements (SREs) within exons. Cassette exons were found to be significantly enriched with A-to-I RNA editing sites compared with constitutive exons. RNA-seq and exon-specific microarray revealed that ADAR knockdown in hepatocarcinoma and myelogenous leukemia cell lines leads to global changes in gene expression, with hundreds of genes changing their splicing patterns in both cell lines. This global change in splicing pattern cannot be explained by putative editing sites alone. Genes showing significant changes in their splicing pattern are frequently involved in RNA processing and splicing activity. Analysis of recently published RNA-seq data from glioblastoma cell lines showed similar results. Our global analysis reveals that ADAR plays a major role in splicing regulation. Although direct editing of the splicing motifs does occur, we suggest it is not likely to be the primary mechanism for ADAR-mediated regulation of alternative splicing. Rather, this regulation is achieved by modulating trans-acting factors involved in the splicing machinery. HepG2 and K562 cell lines were stably transfected with plasmids containing siRNA designed to specifically knock down ADAR expression (ADAR KD). This in order to examine how ADAR affects alternative splicing globally.
2013-06-15 | E-GEOD-47945 | biostudies-arrayexpress
Project description:Alternative mRNA splicing is a major mechanism for gene regulation and transcriptome diversity. Despite the extent of the phenomenon, the regulation and specificity of the splicing machinery are only partially understood. Adenosine-to-inosine (A-to-I) RNA editing of pre-mRNA by ADAR enzymes has been linked to splicing regulation in several cases. Here we used bioinformatics approaches, RNA-seq and exon-specific microarray of ADAR knockdown cells to globally examine how ADAR and its A-to-I RNA editing activity influence alternative mRNA splicing. Although A-to-I RNA editing only rarely targets canonical splicing acceptor, donor, and branch sites, it was found to affect splicing regulatory elements (SREs) within exons. Cassette exons were found to be significantly enriched with A-to-I RNA editing sites compared with constitutive exons. RNA-seq and exon-specific microarray revealed that ADAR knockdown in hepatocarcinoma and myelogenous leukemia cell lines leads to global changes in gene expression, with hundreds of genes changing their splicing patterns in both cell lines. This global change in splicing pattern cannot be explained by putative editing sites alone. Genes showing significant changes in their splicing pattern are frequently involved in RNA processing and splicing activity. Analysis of recently published RNA-seq data from glioblastoma cell lines showed similar results. Our global analysis reveals that ADAR plays a major role in splicing regulation. Although direct editing of the splicing motifs does occur, we suggest it is not likely to be the primary mechanism for ADAR-mediated regulation of alternative splicing. Rather, this regulation is achieved by modulating trans-acting factors involved in the splicing machinery. HepG2 and K562 cell lines were stably transfected with plasmids containing siRNA designed to specifically knock down ADAR expression (ADAR KD). This in order to examine how ADAR affects alternative splicing globally.
2013-06-17 | E-GEOD-47997 | biostudies-arrayexpress
Project description:Filamentous (oomycete and fungal) plant pathogens can deliver cytoplasmic effector proteins into host cells to facilitate disease. How RXLR effectors from the potato late blight pathogen Phytophthora infestans enter host cells is unknown. One possible route involves clathrin-mediated endocytosis (CME). Transient silencing of NbCHC, encoding clathrin heavy chain, or endosome marker NbAra6 in the model host Nicotiana benthamiana, attenuated P. infestans infection and reduced translocation of RXLR effector fusions from transgenic pathogen lines into host cells. In contrast, silencing PP1c isoforms, susceptibility factors that are not required for endocytosis, reduced infection but did not attenuate RXLR effector uptake. Endosome enrichment by ultracentrifugation and sucrose gradient fractionation revealed co-localisation of RXLR effector Pi04314-RFP with clathrin-coated vesicles. Immunopurification of clathrin- and NbAra6-associated vesicles during infection revealed that RXLR effectors Pi04314-RFP and AvrBlb1-RFP, but not apoplastic effector PiSCR74-RFP, were co-immunoprecipitated during infection with pathogen lines secreting these effectors. MS/MS analyses of proteins co-immunoprecipitated with NbAra6-GFP during infection revealed enrichment of host proteins associated with endocytic vesicles alongside multiple pathogen RXLR effectors, but not apoplastic effectors, including PiSCR74, which do not enter host cells. Our data show that uptake of P. infestans RXLR effectors into plant cells occurs via CME.
2023-07-20 | PXD040285 | Pride