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PAMP-triggered genetic reprogramming involves widespread alternative transcription initiation and an immediate transcription factor wave

ABSTRACT: Immune responses triggered by pathogen-associated molecular patterns (PAMPs) are key to pathogen defense, but drivers and stabilizers of the growth-to-defense genetic reprogramming remain incompletely understood in plants. Here, we report a time-course study of the establishment of PAMP-triggered immunity (PTI) using cap analysis of gene expression. We show that around 15% of all transcription start sites (TSSs) rapidly induced during PTI define alternative transcription initiation events. From these, we identify clear examples of regulatory TSS change via alternative inclusion of target peptides or domains in encoded proteins, or of upstream open reading frames in mRNA leader sequences. We also find that 60% of PAMP response genes respond earlier than previously thought. In particular, a cluster of rapidly and transiently PAMP-induced genes is enriched in transcription factors (TFs) whose functions, previously associated with biological processes as diverse as abiotic stress adaptation and stem cell activity, appear to converge on growth restriction. Furthermore, examples of known potentiators of PTI, in one case under direct mitogen-activated protein kinase control, support the notion that the rapidly induced TFs could constitute direct links to PTI signaling pathways and drive gene expression changes underlying establishment of the immune state.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE144356 | GEO | 2021/12/15

REPOSITORIES: GEO

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PAMP-triggered genetic reprogramming involves widespread alternative transcription initiation and an immediate transcription factor wave

Project description:Immune responses triggered by pathogen-associated molecular patterns (PAMPs) are key to pathogen defense, but drivers and stabilizers of the growth-to-defense genetic reprogramming remain incompletely understood in plants. Here, we report a time-course study of the establishment of PAMP-triggered immunity (PTI) using cap analysis of gene expression. We show that around 15% of all transcription start sites (TSSs) rapidly induced during PTI define alternative transcription initiation events. From these, we identify clear examples of regulatory TSS change via alternative inclusion of target peptides or domains in encoded proteins, or of upstream open reading frames in mRNA leader sequences. We also find that 60% of PAMP response genes respond earlier than previously thought. In particular, a cluster of rapidly and transiently PAMP-induced genes is enriched in transcription factors (TFs) whose functions, previously associated with biological processes as diverse as abiotic stress adaptation and stem cell activity, appear to converge on growth restriction. Furthermore, examples of known potentiators of PTI, in one case under direct mitogen-activated protein kinase control, support the notion that the rapidly induced TFs could constitute direct links to PTI signaling pathways and drive gene expression changes underlying establishment of the immune state.

2021-12-15 | GSE143590 | GEO

Role of MPK4 in pathogen-associated molecular pattern-triggered alternative splicing in Arabidopsis

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.

2020-03-03 | GSE146189 | GEO

The Arabidopsis miR396 mediates pathogen-associated molecular pattern-triggered immune responses against fungal pathogens

Project description:A first line of defense against pathogen infections is the recognition of pathogen-associated molecular patterns (PAMPs), leading to PAMP-triggered immunity (PTI). MicroRNAs (miRNAs) are primarily known as central regulators of plant development, but a few have also been connected to immunity. We have found that several fungal pathogens lead to a reduction in miR396 levels, suggesting that miR396 are negative regulators of downstream defense responses. In agreement with such as scenario, constitutive attenuation of miR396 activity enhances resistance to infection by fungal pathogens, while increased miR396 activity reduces pathogen resistance. We conclude that constitutive reduction of miR396 levels confer a primed state for enhanced defense reactions

2017-02-28 | GSE76819 | GEO

O antigen acts as a shield to delay early plant immune recognition of the pathogenic bacterium, Xylella fastidiosa

Project description:PAMP-triggered immunity (PTI) is the first line of plant defense against invading organisms. Initiated through the perception of conserved pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide or flagellin, PTI can provide early protection against a broad range of pathogens. Active suppression of PTI by microbial effector proteins, particularly those secreted by the Type III secretion system (T3SS), is a well-known strategy employed by bacterial plant pathogens that enables them to subvert PTI and successfully colonize their hosts. In this study, we demonstrate that the xylem-limited bacterium, Xylella fastidiosa, which lacks a T3SS, utilizes an alternative strategy to delay elicitation of innate immune responses. By decorating its LPS PAMP molecule with a high molecular weight O antigen, this bacterium physically masks itself from early recognition by the grapevine innate immune system. We have elucidated the chemical structure of the O antigen and found that it is primarily an α1,2-linked rhamnan polymer. X. fastidiosa cells lacking O antigen elicited hallmarks of PTI such as ROS production, specifically in the plant xylem tissue compartment, which is comprised primarily of non-living cells. By coupling histological and genome-wide transcriptional profiling, we demonstrate that X. fastidiosa lacking its O antigen shield activates defense-related genes in grapevine. This includes a stronger and more prolonged oxidative burst at concentrations high enough to inhibit pathogen proliferation. To begin exploring translational applications of our findings, we also demonstrate that purified X. fastidiosa LPS elicitor can prime grapevine defenses, thereby conferring host tolerance to subsequent challenge with X. fastidiosa.

2018-02-22 | GSE87643 | GEO

Proteomics of different types of immunity in potato

Project description:Plants have a wide variety of ways to defend against pathogens. A commonly used model of the plant immune system divides it into a general response triggered by pathogen associated molecular patterns (PAMPs) and a specific response triggered by effectors. The first type of response is known as PAMP triggered immunity (PTI) and the second as effector-triggered immunity (ETI). We have performed a proteomical analysis of one PTI and two ETI models in potato and compared their effect on protein expression.

2019-10-17 | PXD012576 | Pride

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

2022-10-12 | PXD036739 | Pride

Naked1 targets Topless to up-regulate Auxin signaling and suppress immunity

Project description:Plants integrate endogenous and environmental signals to regulate growth and developmental programs by the use different hormonal pathways. Perception of Pathogen/Microbial Associated Molecular Patterns (PAMPs/MAMPs) from invading microorganisms triggers a series of defense reactions known as Pathogen Triggered Immunity (PTI) that inhibit growth promoting signaling pathways such as auxin signaling. On the contrary, pathogens manipulate growth signaling and metabolism to promote disease susceptibility, but how this hormone acts on immunity is not fully understood. Ustilago maydis is a fungal pathogen of maize. Infected plants show formation of galls, masses of undifferentiated tissue, and upregulation of auxin signaling. Here we show that a secreted protein from U. maydis, the effector Naked1 (Nkd1), translocates into the host nucleus where it interacts with members of the Topless/Topless related family of transcriptional co-repressors. Nkd1 binds to TPL/TPRs through its native EAR motif and prevents recruitment of transcriptional repressors involved in hormonal signaling, leading to the de-repression of jasmonic acid and auxin responsive genes. We show that up-regulation of auxin signaling leads to inhibition of PAMP-triggered ROS burst, one of the earliest PTI responses, and increased susceptibility to pathogens. Thus, establishing a clear mechanism for auxin-induced pathogen susceptibility. Using engineered variants of Nkd1, with altered affinity/specificity to TPL/TPRs, we show that increased EAR-mediated binding triggers typical salicylic acid mediated defense reactions, leading to pathogen resistance.

2021-06-01 | GSE141597 | GEO

The proteasome acts as a hub for local and systemic plant immunity in Arabidopsis thaliana and constitutes a virulence target of Pseudomonas syringae type-III effector proteins

Project description:Recent evidence suggests that the ubiquitin-proteasome system (UPS) is involved in several aspects of plant immunity and a range of plant pathogens subvert the UPS to enhance their virulence. Here we show that proteasome activity is strongly induced during basal defense in Arabidopsis. Mutant lines of the proteasome subunits RPT2a and RPN12a support increased bacterial growth of virulent Pseudomonas syringae pv. tomato DC3000 (Pst) and Pseudomonas syringae pv. maculicola ES4326. Both proteasome subunits are required for Pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI) responses. Analysis of bacterial growth after a secondary infection of systemic leaves revealed that the establishment of systemic-acquired resistance (SAR) is impaired in proteasome mutants, suggesting that the proteasome also plays an important role in defense priming and SAR. In addition, we show that Pst inhibits proteasome activity in a type-III secretion dependent manner. A screen for type-III effector proteins from Pst for their ability to interfere with proteasome activity revealed HopM1, HopAO1, HopA1 and HopG1 as putative proteasome inhibitors. Biochemical characterization of HopM1 by mass-spectrometry indicates that HopM1 interacts with several E3 ubiquitin ligases and proteasome subunits. This supports the hypothesis that HopM1 associates with the proteasome leading to its inhibition. Thus, the proteasome is an essential component of PTI and SAR, which is targeted by multiple bacterial effectors.

2017-10-09 | PXD004883 | Pride

An immune-inducible trihelix transcription factor suppresses bacterial resistance in Arabidopsis thaliana

Project description:The plant innate immunity consists of the two interconnected mechanisms, pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Although much is known about how plants trigger immune responses upon pathogen recognition, the genetic program by which plants avoid an overshoot in pathogen-triggered immune responses remains largely unknown. Here, we discovered a trihelix transcription factor, GT-3a, as an immune-inducible negative regulator of bacterial resistance in Arabidopsis thaliana. Analysis of public RNA-seq data revealed that GT-3a is specifically induced by ETI activation not by PTI activation. Overexpression of GT-3a suppressed resistance against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (Pto) and Pto-elicited expression of salicylic acid (SA)-responsive genes. Our results suggest that transcriptional induction of GT-3a circumvents the overshooting of SA-mediated defense responses during ETI.

2024-02-18 | GSE248054 | GEO

tRNA-seq of Arabidopsis leaves during pattern-triggered immunity

Project description:During pattern-triggered immunity (PTI), the first line of active defense against infection in plants, the translatome undergoes rapid reprogamming. To understand how defense proteins are selectively translated, we conducted a genetic screen for regulators of PTI using a translational reporter. We identified a mutant of RNA helicase 12 (RH12) showing compromised reporter translation and pathogen resistance. RH12 is a homolog of yeast DEAD-box Helicase Homolog 1, which targets mRNAs with low codon optimality for decay. Therefore, we sequenced the Arabidopsis tRNAome to determine codon optimality during PTI. We discovered a PTI-associated reduction in overall codon optimality of the transcriptome, and found that the decay of transcripts with reduced optimality is mediated by interaction with RH12. Our results demonstrate the first example of codon optimality-associated decay as part of an adaptive response in which the dynamics of both the tRNAome and the transcriptome facilitate rapid changes in translational output during PTI.

2023-04-02 | GSE171411 | GEO

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