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Transcriptome profiling of LecRKVI.2 over-expressor plants.

ABSTRACT: The arabidopsis L-type lectin receptor kinase-VI.2 positively regulates bacterial PAMP-triggered immunity. We used microarrays and performed genome-wide transcriptome analysis of LecRKVI.2 over-expressing plants and identified number of upregulated genes involved against bacterial resistance.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE26646 | GEO | 2012/03/19

SECONDARY ACCESSION(S): PRJNA136377

REPOSITORIES: GEO

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Transcriptome profiling of LecRKVI.2 over-expressor plants.

Project description:The arabidopsis L-type lectin receptor kinase-VI.2 positively regulates bacterial PAMP-triggered immunity. We used microarrays and performed genome-wide transcriptome analysis of LecRKVI.2 over-expressing plants and identified number of upregulated genes involved against bacterial resistance. Total RNA was isolated from 5-week-old Arabidopsis plants for RNA extraction and hybridisation on Affymetrix microarrays.

2012-03-19 | E-GEOD-26646 | biostudies-arrayexpress

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Project description:Alternative splicing (AS) of pre-mRNAs in plants is an important mechanism of gene regulation in environmental stress tolerance but plant signals involved are essentially unknown. Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) is mediated by mitogen-activated protein kinases and the majority of PTI defense genes are regulated by MPK3, MPK4 and MPK6. These responses have been mainly analyzed at the transcriptional level, however many splicing factors are direct targets of MAPKs. Here, we studied alternative splicing induced by the PAMP flagellin in Arabidopsis.

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The Arabidopsis E3 ubiquitin ligase PUB4 regulates BIK1 and is targeted by a bacterial type-III effector

Project description:Plant immunity is tightly controlled by a complex and dynamic regulatory network, which ensures optimal activation upon detection of potential pathogens. Accordingly, each component of this network is a potential target for manipulation by pathogens. Here, we report that RipAC, a type III-secreted effector from the bacterial pathogen Ralstonia solanacearum, targets the plant E3 ubiquitin ligase PUB4 to inhibit pattern-triggered immunity (PTI). PUB4 plays a positive role in PTI by regulating the homeostasis of the central immune kinase BIK1. Before PAMP perception, PUB4 promotes the degradation of non-activated BIK1, while, after PAMP perception, PUB4 contributes to the accumulation of activated BIK1. RipAC leads to BIK1 degradation, which correlates with its PTI-inhibitory activity. RipAC causes a reduction in pathogen-associated molecular pattern (PAMP)-induced PUB4 accumulation and phosphorylation. Our results shed light on the role played by PUB4 in immune regulation, and illustrate an indirect targeting of the immune signalling hub BIK1 by a bacterial effector

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Project description:Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI) are well-defined modes of plant immunity triggered by recognition of pathogen effector proteins and microbe-associated molecular patterns, respectively. While ETI and PTI network extensively share signaling components, the shared components are used in different ways, resulting in distinct network properties in the model plant Arabidopsis: immunity is highly robust against network perturbations in ETI but relatively sensitive in PTI. However, the molecular mechanism how the shared network leads to the different properties is not known. Here we show that sustained MAPK activation compensate salicylic acid (SA) signaling. A 12 DNA microarray study using total RNA from Arabidopsis transgenic plants carrying DEX-inducible MKK4DD in Col or sid2-2 background treated with DEX or control.

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