Transcription profiling of Arabidopsis leading to the identification of novel components in the EDS1/PAD4-regulated defence pathwayabidopsis-Pst-eds1-pad4
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
SUBMITTER: Svenja Debey
PROVIDER: E-MEXP-546 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Salicylic acid-independent ENHANCED DISEASE SUSCEPTIBILITY1 signaling in Arabidopsis immunity and cell death is regulated by the monooxygenase FMO1 and the Nudix hydrolase NUDT7.
Bartsch Michael M Gobbato Enrico E Bednarek Pawel P Debey Svenja S Schultze Joachim L JL Bautor Jaqueline J Parker Jane E JE
The Plant cell 20060310 4
Arabidopsis thaliana ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) controls defense activation and programmed cell death conditioned by intracellular Toll-related immune receptors that recognize specific pathogen effectors. EDS1 is also needed for basal resistance to invasive pathogens by restricting the progression of disease. In both responses, EDS1, assisted by its interacting partner, PHYTOALEXIN-DEFICIENT4 (PAD4), regulates accumulation of the phenolic defense molecule salicylic acid (SA) and oth ...[more]
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Project description:In the absence of adaptive immunity displayed by animals, plants respond locally to biotic challenge via inducible basal defense networks activated through recognition and response toconserved pathogen associated molecular patterns (PAMPs). In addition, immunity can be induced in tissues remote from infection sites via systemic acquired resistance (SAR), initiated following gene-for-gene recognition between plant resistance proteins and microbial effectors.The nature of the mobile signal and remotely activated networks responsible for establishing SAR remain unclear. Here we show that despite the absence of PAMP contact, systemically responding leaves rapidly activate a SAR transcriptional signature with strong similarity to local basal defense. Jasmonates have previously been implicated in systemic signalling in response to wounding and plant herbivory but not SAR. We present several lines of evidence that suggest jasmonates may also be central to SAR. Jasmonic acid (JA) rapidly accumulates in phloem exudates of leaves challenged with an avirulent strain of Pseudomonas syringae. In systemically responding leaves transcripts associated with jasmonate biosynthesis are upregulated and JA increases transiently. SAR can be mimicked by foliar JA application and is abrogated in mutants impaired in jasmonate synthesis or response. We conclude that, jasmonate signalling appears to mediate long-distance information transmission. Moreover, the systemic transcriptional response shares extraordinary overlap with local herbivory and wounding responses, indicating that jasmonates may be central to an evolutionarily conserved signalling network, which decodes multiple abiotic and biotic stress signals. Experimenter name: William Truman; Experimenter phone: +44 (0)1392 263789; Experimenter fax: +44 (0)1392 263434; Experimenter address: School of Biosciences; Experimenter address: Geoffrey Pope Building; Experimenter address: Stocker Road; Experimenter address: Exeter; Experimenter address: Devon; Experimenter zip/postal_code: EX4 4QD; Experimenter country: UK Experiment Overall Design: 9 samples were used in this experiment
2008-06-15 | E-GEOD-6831 | biostudies-arrayexpress
Project description:Nod-like receptors (NLRs) belong to AAA+ ATPases and act as ATP-dependent molecular switches, which detect activity of pathogens. Function of a large class of plant NLRs with Toll-like domain (TNL) is fully dependent on a class of EDS1-like proteins specific to seed plants. EDS1 (Enhanced Disease Susceptibility 1) – like proteins are defined as fusions of two domains: lipase-like a/b hydrolase domain and an a-helical bundle domain specific to the EDS1 family. In Arabidopsis, RRS1-RPS4 TNL signaling is dependent on the nuclear localization of EDS1 and formation of heterodimers between EDS1 and its sequence-related partners, PAD4 and SAG101. Here, we deposited results of affinity purification and LC-MS analyses are deposited for the EDS1 complexes after triggering NLR-dependent immune responses in Arabidopsis leaves. As a negative control, plants expressing GFP-tagged Telomere Repeat Binding 1 were used. The complexes were purified from nuclear enriched fractions of Arabidopsis complementation lines infected with the TNL-triggering bacteria.
2021-04-06 | PXD025202 | Pride
Project description:There is growing evidence that for a comprehensive insight into the function of plant genes it is crucial to assess their functionalities under a wide range of conditions. In this study we examined the role of LESION SIMULATING DISEASE1 (LSD1), ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4) in the regulation of photosynthesis, water use efficiency (WUE), ROS/hormonal homeostasis and seed yield in Arabidopsis thaliana grown in the laboratory and in the field. We demonstrate that the LSD1 null mutant (lsd1), which is known to exhibit a runaway cell death in non-permissive conditions, proves to be more tolerant to combined drought and high-light stress than the wild type. Moreover, depending on growing conditions, it shows variations in WUE, salicylic acid and hydrogen peroxide concentrations, photosystem II maximum efficiency and in transcription profiles. However, despite these changes, lsd1 demonstrates similar seed yield under all tested conditions. All of these traits depend on EDS1 and PAD4. The differences in the pathways prevailing in the lsd1 in various growing environments are manifested by the significantly smaller number of transcripts deregulated in the field compared to the laboratory, with only 43 commonly regulated genes. Our data indicate that LSD1, EDS1 and PAD4 participate in the regulation of various molecular and physiological processes that influence Arabidopsis fitness. On the basis of these results we emphasize that the function of such important regulators as LSD1, EDS1 and PAD4 should be studied not only under stable laboratory conditions, but also in the environment abounding in multiple stresses. Six genotypes x two conditions experiment including five-week-old WT (Ws), lsd1, pad4, eds1, eds1lsd1, and pad4lsd1 plants grown in laboratory or field conditions, hybridized in two loop-designs (lab and field). Two biological replicates. In total, 2 x 12 samples were hybridized on 24 Arabidopsis Gene Expression microarrays V4 (Agilent, two-color array) including color swap of replicate samples.
2013-02-07 | E-GEOD-24766 | biostudies-arrayexpress
Project description:Our previous study on CBP60g, a calmodulin binding protein that is important for disease resistance and microbe-associated molecular pattern (MAMP)-induced SA accumulation, led to our discovery of a closely related family member CBP60h. CBP60h is also important for defense against P. syringae but is induced differently by pathogen and MAMP stimulus. Transcriptome profiling of cbp60h mutants suggested that CBP60h might be primarily functioning in response against P. syringae. We constructed a double mutant of cbp60g and cbp60h, which demonstrated severely defective defense against P. syringae and SA accumulation. Profiling of the cbp60g/h showed that its expression pattern is very similar to that of pad4. Transient expression in Tobacco showed that both CBP60g and CBP60h localized to nucleus. Our observation suggest that CBP60g and CBP60h share partially redundant but critical role in defense response and SA signaling. This experiment consists of three biological replicates. For each genotype, two leaves per plant were pooled from three pots to prepare total RNA.
2009-11-03 | E-GEOD-18865 | biostudies-arrayexpress
Project description:Arabidopsis Enhanced Disease Susceptibility 1 (EDS1) and its direct partner Phytoalexin Deficient 4 (PAD4) are required for both basal resistance against virulent pathogens and innate immune responses mediated by all tested TIR (Toll-Interleukin-1 Receptors) type nucleotide-binding/leucine-rich-repeat (NLR) receptors. Using transgenic Arabidopsis plants in Col-0 eds1-2 pad4-1 background conditionally expressing PAD4 and constitutively expressing EDS1 (ED-P4E1), an EDS1/PAD4 immune response can be triggered by estradiol treatment and can induce expression of defense-related genes and lead to enhanced basal resistance. In order to capture primary transcriptional changes in response to EDS1/PAD4, we performed RNA-seq gene expression analysis in ED-P4E1 plants after estradiol or mock treatment at three time points: 6, 12 and 24 h.
2016-09-27 | GSE80585 | GEO
Project description:Arabidopsis pathogen effector-triggered immunity (ETI) is controlled by a family of three lipase-like proteins EDS1, PAD4 and SAG101 and two sub-families of HET-S/LOB-B (HeLo)-domain “helper” NLRs, ADR1s and NRG1s. EDS1-PAD4 dimers cooperate with ADR1s, and EDS1-SAG101 dimers with NRG1s, in two separate defense-promoting modules. EDS1-PAD4-ADR1 and EDS1- SAG101-NRG1 complexes were detected in immune-activated leaf extracts but the molecular determinants for specific complex formation and function remain unknown. EDS1 signaling is mediated by a C-terminal EP domain (EPD) surface surrounding a cavity formed by the heterodimer. Here we investigated whether the EPDs of PAD4 and SAG101 contribute to EDS1 dimer functions. Using a structure-guided approach, we undertook a comprehensive mutational analysis of Arabidopsis PAD4. We identify two conserved residues (Arg314 and Lys380) lining the PAD4 EPD cavity that are essential for EDS1-PAD4 mediated pathogen resistance, but are dispensible for PAD4 mediated restriction of green peach aphid infestation. Positionally equivalent Met304 and Arg373 at the SAG101 EPD cavity are required for EDS1-SAG101 promotion of ETI-related cell death. In a PAD4 and SAG101 interactome analysis of ETI-activated tissues, PAD4R314A and SAG101M304R EPD variants maintain interaction with EDS1 but lose association, respectively, with helper NLRs ADR1-L1 and NRG1.1, and other immune-related proteins. Our data reveal a fundamental contribution of similar but non-identical PAD4 and SAG101 EPD surfaces to specific EDS1 dimer protein interactions and pathogen immunity.
2022-03-17 | PXD029477 | Pride
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2010-05-07 | E-GEOD-14237 | biostudies-arrayexpress
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2021-04-06 | PXD021301 | Pride
Project description:We present here the transcriptominc changes occuring after TNL-triggered immunity after infection with pst AvrRps4 in a point mutant of EDS1, EDS1-R493A
2019-02-26 | GSE116269 | GEO