Expression profiling of Fusarium oxysporum infected wild-type Arabidopsis and a 35S Fusarium SIX4 overexpression line.
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE75928 | GEO | 2016/05/31
SECONDARY ACCESSION(S): PRJNA305746
REPOSITORIES: GEO
Similar Datasets
Project description:Fungal effectors play important roles in inciting disease development on host plants. We identified an effector (Secreted in Xylem4, SIX4) in an Arabidopsis infecting isolate (Fo5176) of the root-infecting fungal pathogen Fusarium oxysporum and demonstrated this effector is required for full virulence. To explore the role of Fo5176_SIX4 we use whole transcriptome profiling of root tissues from plants overexpressing this effector (35sSIX4) versus wild-type (Col-0) plants after F. oxysporum infection. We grew both WT and 35sSIX4 plants for four weeks in soil. After four weeks the plants were infected with Fusarium oxyporum isolate Fo5176, trays covered with a plastic dome and incubated at 28C. There were four independent replicates of each treatment and each replicate contained root tissue from 20 plants. Each replicate (8 in total) was harvested 4 days post inoculation and the resulting RNA was used for hybridization to an Affymetrix ATH1 chip.
2016-05-31 | E-GEOD-75928 | biostudies-arrayexpress
Project description:The Mediator complex is an evolutionary conserved multiprotein complex that plays an essential role in initiating and regulating transcription. Its function is to act as a universal adaptor between RNA Polymerase II and DNA-bound transcription factors to translate regulatory information from activators and repressors to the transcriptional machinery. We have found that the PFT1 gene (which encodes the MED25 subunit of the Mediator complex) is required for the uncompromised expression of both salicylic acid- and jasmonate-dependent defense genes as well as resistance to the leaf-infecting fungal pathogens, Alternaria brassicicola and Botrytis cinerea in Arabidopsis. Surprisingly, we found that the pft1/med25 mutant showed increased resistance to the root infecting pathogen Fusarium oxysporum and that this resistance was independent of classical defense genes. In addition, the over-expression of PFT1 led to increased susceptibility to F. oxysporum. Therefore, to explore this phenomenon further, we wished to use whole genome transcript profiling to identify which genes may be playing a role in pft1/med25-mediated resistance to F. oxysporum. Experiment Overall Design: We grew both WT and pft1/med25 plants for four weeks in soil. After four weeks we treated the plants by root-dipping in either water or a F. oxysporum spore suspension before replanting them back into soil. There were four independent replicates of each treatment and each replicate contained 20 plants each. The treatments were WT (mock): pft1 (mock): WT (infected): pft1 (infected). Each replicate (16 in total) was harvested after 48 hours and the resulting RNA was used for hybridization to an Affymetrix ATH1 chip.
2009-09-05 | E-GEOD-15236 | biostudies-arrayexpress
Project description:The Mediator complex is an evolutionary conserved multiprotein complex that plays an essential role in initiating and regulating transcription. Its function is to act as a universal adaptor between RNA Polymerase II and DNA-bound transcription factors to translate regulatory information from activators and repressors to the transcriptional machinery. We have found that the PFT1 gene (which encodes the MED25 subunit of the Mediator complex) is required for the uncompromised expression of both salicylic acid- and jasmonate-dependent defense genes as well as resistance to the leaf-infecting fungal pathogens, Alternaria brassicicola and Botrytis cinerea in Arabidopsis. Surprisingly, we found that the pft1/med25 mutant showed increased resistance to the root infecting pathogen Fusarium oxysporum and that this resistance was independent of classical defense genes. In addition, the over-expression of PFT1 led to increased susceptibility to F. oxysporum. Therefore, to explore this phenomenon further, we wished to use whole genome transcript profiling to identify which genes may be playing a role in pft1/med25-mediated resistance to F. oxysporum.
2009-08-24 | GSE15236 | GEO
Project description:Jasmonate (JA) signaling plays a key role in mediating both resistance and susceptibility to the root-infecting fungal pathogen Fusarium oxysporum. Within this system, the roles of the JA-signaling repressor gene family of JASMONATE ZIM-domain (JAZ) genes had not been investigated. By screening JAZ T DNA insertion lines for altered resistance or susceptibility to F. oxysporum, we identified a JAZ7 mutant (jaz7-1D) highly susceptible to F. oxysporum infection. Further analyses revealed jaz7-1D exhibits constitutively active JAZ7 expression, enhanced expression of JA-defense marker genes, and increased sensitivity to JA-inhibition of root elongation. To further explore altered JA-signaling and JA-responses in this mutant, we use whole transcriptome profiling of jaz7-1D versus wild-type (Col-0) plants after mock/control and JA treatment.
2016-02-08 | GSE61884 | GEO
Project description:In plant pathogenic fungi, conditionally dispensable (CD) chromosomes are often associated with virulence, but not viability. Such virulence-associated CD chromosomes carry genes encoding effectors and/or host-specific toxin biosynthesis enzymes, potentially important for determining host specificity. Fusarium oxysporum causes devastating diseases of more than 100 plant species. In particular, F. oxysporum f. sp. conglutinans (Focn) can infect Brassicaceae plants including Arabidopsis and cabbage. Here we show that Focn has multiple CD chromosomes involving in not only virulence but also vegetative growth, which is an atypical feature of known CD chromosomes. Among them, we identified specific CD chromosomes that are required for virulence to either Arabidopsis, cabbage, or both. We revealed that a pair of effectors encoded in one of the CD chromosomes is required for suppression of the Arabidopsis-specific phytoalexin-based immunity. The effector pair is highly conserved in F. oxysporum isolates capable of infecting Arabidopsis. This study provides insights into how host specificity of F. oxysporum is determined by a pair of effector genes on a CD chromosome.
2021-06-16 | GSE157823 | GEO
Project description:The influence of during colonization by Fusarium oxysporum f. sp. Lycopersici secreted effector proteins on the proteome of the xylem sap of tomato plants was investigated using a label-free quantitative proteomics approach. A comparison was made between plants inoculated with either a mock control, a non-effector knockout control, Fusarium oxysporum Fol007 wildtype and four Fol007 single effector protein knockout strains. Specific effects on the relative abundance of certain proteins of the xylem sap occurred for the different knockout strains next to a core set of 24 differentially accumulated proteins which may provide insights into the mechanisms of promoting infection for each of the tested effector proteins.
2015-10-26 | PXD003010 | Pride
Project description:Jasmonate (JA) signaling plays a key role in mediating both resistance and susceptibility to the root-infecting fungal pathogen Fusarium oxysporum. Within this system, the roles of the JA-signaling repressor gene family of JASMONATE ZIM-domain (JAZ) genes had not been investigated. By screening JAZ T DNA insertion lines for altered resistance or susceptibility to F. oxysporum, we identified a JAZ7 mutant (jaz7-1D) highly susceptible to F. oxysporum infection. Further analyses revealed jaz7-1D exhibits constitutively active JAZ7 expression, enhanced expression of JA-defense marker genes, and increased sensitivity to JA-inhibition of root elongation. To further explore altered JA-signaling and JA-responses in this mutant, we use whole transcriptome profiling of jaz7-1D versus wild-type (Col-0) plants after mock/control and JA treatment. We grew both WT and jaz7-1D plants for four weeks in soil. After four weeks the plants were treated with 1 mL of 5% MeJA (dissolved in 100% ethanol) or 1 mL of Mock solution (100% ethanol) by applying the solutions to a cotton ball attached to a tray cover which was then used to enclose individual trays. Each tray and cover was then sealed by two layers of opaque plastic bags and secured with masking tape. There were four independent replicates of each treatment and each replicate contained leaf tissue from 20 plants. Each replicate (16 in total) was harvested after 6 hours and the resulting RNA was used for hybridization to an Affymetrix ATH1 chip.
2016-02-08 | E-GEOD-61884 | biostudies-arrayexpress
Project description:Fusarium oxysporum is one of the most common species causing soybean root rot and seedling blight in the U.S. In a recent study, significant variation in aggressiveness was observed among isolates of F. oxysporum collected from roots in Iowa, ranging from highly pathogenic to weakly or non-pathogenic isolates. In the present work, a RNA-seq-based analysis was used for the first time to investigate the molecular aspect of the interaction of a partially resistant soybean genotype with non-pathogenic/pathogenic isolates of F. oxysporum at 72 and 96 hours post inoculation (hpi). Markedly different gene expression profiles were observed in compatible and incompatible host-pathogen combinations. A peak of differentially expressed genes (DEGs) was observed at 72 hpi in soybean roots in response to both isolates, although the number of DEGs was about eight times higher for the pathogenic isolate compared to the non-pathogenic one (1,659 vs. 203 DEGs, respectively). Furthermore, not only the number of genes, but also the magnitude of induction was much greater in response to the pathogenic isolate. This response included a stronger activation of many well-known defense-related genes, and several genes involved in ethylene biosynthesis and signalling, transcription factors, secondary and sugar metabolism. In addition, 1130 fungal genes were differentially expressed between the F. oxysporum isolates in planta during the infection process. Interestingly, 10% of these genes encode plant cell-wall degrading enzymes, reactive oxygen species-related enzymes and fungal proteins involved in primary metabolic pathways. Such information may be useful in the development of new methods of broadening resistance of soybean to F. oxysporum, including the silencing of important fungal genes, and also to understand the molecular basis of soybean-F. oxysporum interactions. Soybean seedlings mRNA profiles inoculated with a non-pathogenic and pathogenic isolates of F. oxysporum and collected at 72 and 96 hpi, were generated using Illumina HiSeq 2500. Control seedlings were also included for each time of inoculation. Three biological replicates were considered for each condition, 18 samples in total.
2016-03-31 | E-GEOD-66861 | biostudies-arrayexpress
Project description:Soilborne fungal pathogens cause devastating yield losses, are highly persistent and difficult to control. To culminate infection, these organisms must cope with limited availability of iron. Here we show that the bZIP protein HapX functions as a key regulator of iron homeostasis and virulence in the vascular wilt fungus Fusarium oxysporum. Deletion of hapX does not affect iron uptake, but causes derepression of genes involved in iron-consuming pathways, leading to impaired growth under iron-depleted conditions. F. oxysporum strains lacking HapX are reduced in their capacity to invade and kill tomato plants and immunodepressed mice. The virulence defect of ΔhapX on tomato plants is exacerbated by coinoculation of roots with a biocontrol strain of Pseudomonas putida, but not with a siderophore-deficient mutant, indicating that HapX contributes to iron competition of F. oxysporum in the tomato rhizosphere. These results establish a conserved role for HapX-mediated iron homeostasis in fungal infection of plants and mammals.
2012-07-14 | GSE39325 | GEO
Project description:Soilborne fungal pathogens cause devastating yield losses, are highly persistent and difficult to control. To culminate infection, these organisms must cope with limited availability of iron. Here we show that the bZIP protein HapX functions as a key regulator of iron homeostasis and virulence in the vascular wilt fungus Fusarium oxysporum. Deletion of hapX does not affect iron uptake, but causes derepression of genes involved in iron-consuming pathways, leading to impaired growth under iron-depleted conditions. F. oxysporum strains lacking HapX are reduced in their capacity to invade and kill tomato plants and immunodepressed mice. The virulence defect of M-NM-^ThapX on tomato plants is exacerbated by coinoculation of roots with a biocontrol strain of Pseudomonas putida, but not with a siderophore-deficient mutant, indicating that HapX contributes to iron competition of F. oxysporum in the tomato rhizosphere. These results establish a conserved role for HapX-mediated iron homeostasis in fungal infection of plants and mammals. Iron dependent gene expression in Fusarium oxysporum wt and M-NM-^ThapX mutant was measured 1 hour after shifting the mycelia to minimal medium with or without 50 M-NM-<M Fe2(SO4)3. Three independent experiments were performed.
2012-07-13 | E-GEOD-39325 | biostudies-arrayexpress