Expression analysis of Arabidopsis peptidoglycan (PGN) recognition mutants treated with PGN
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE28004 | GEO | 2011/11/10
SECONDARY ACCESSION(S): PRJNA137787
REPOSITORIES: GEO
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Project description:Recognition of microbial patterns by host pattern recognition receptors is a key step in immune activation in multicellular eukaryotes. Peptidoglycans (PGN) are major components of bacterial cell walls and possess immunity-stimulating activities in metazoans and plants. Here, we show that PGN sensing in Arabidopsis thaliana requires three LysM domain proteins, LYM1, LYM3 and CERK1. A 24 DNA microarray study using toral RNA from three Arabidopsis mutants (lym1-1, lym3-1, cerk1-2) as well as wild type treated with water or peptidoglycan.
2011-11-10 | E-GEOD-28004 | biostudies-arrayexpress
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Project description:The LysM-RLK CERK1 is a major chitin binding protein in Arabidopsis thaliana and subject to chitin-induced phosphorylation
2010-10-21 | PRD000289 | Pride
Project description:Pattern-recognition receptor (PRR)-triggered immunity (PTI) plays a pivotal role in plant immunity to ward off a wide range of pathogenic microbes. The model liverwort Marchantia polymorpha is gaining popularity in investigating the evolution of plant-microbe interactions. The M. polymorpha is capable of triggering defense-related gene expression by sensing components in bacterial and fungal extracts, suggesting existence of PTI in this plant model. However, the molecular components that would form PTI in M. polymorpha have not yet been described. We show that, in M. polymorpha, lysin motif (LysM) receptor-like kinase (LYK) MpLYK1 and LYK-related (LYR) MpLYR, among four LysM receptor homologs, are required for sensing chitin and peptidoglycan (PGN) fragments and thereby triggering a series of immune responses. Phosphoproteomic analysis of M. polymorpha in response to chitin treatment comprehensively identified regulatory proteins that would shape LysM-mediated PTI. The identified proteins covered homologs of well-described PTI components in angiosperms as well as proteins whose roles in PTI are not yet determined including the blue-light receptor phototropin MpPHOT. We revealed that MpPHOT is required for a negative feedback of defense-related gene expression during PTI. Taken together, this study provides the basic framework of LysM-mediated PTI in M. polymorpha and demonstrates the utility of M. polymorpha as a plant model for discovering novel or fundamental molecular mechanisms underlying PRR-triggered immune signaling in plants.
2023-11-06 | PXD042084 | Pride
Project description:Pattern-recognition receptor (PRR)-triggered immunity (PTI) plays a pivotal role in plant immunity to ward off a wide range of pathogenic microbes. The model liverwort Marchantia polymorpha is gaining popularity in investigating the evolution of plant-microbe interactions. The M. polymorpha is capable of triggering defense-related gene expression by sensing components in bacterial and fungal extracts, suggesting existence of PTI in this plant model. However, the molecular components that would form PTI in M. polymorpha have not yet been described. We show that, in M. polymorpha, lysin motif (LysM) receptor-like kinase (LYK) MpLYK1 and LYK-related (LYR) MpLYR, among four LysM receptor homologs, are required for sensing chitin and peptidoglycan (PGN) fragments and thereby triggering a series of immune responses. Phosphoproteomic analysis of M. polymorpha in response to chitin treatment comprehensively identified regulatory proteins that would shape LysM-mediated PTI. The identified proteins covered homologs of well-described PTI components in angiosperms as well as proteins whose roles in PTI are not yet determined including the blue-light receptor phototropin MpPHOT. We revealed that MpPHOT is required for a negative feedback of defense-related gene expression during PTI. Taken together, this study provides the basic framework of LysM-mediated PTI in M. polymorpha and demonstrates the utility of M. polymorpha as a plant model for discovering novel or fundamental molecular mechanisms underlying PRR-triggered immune signaling in plants.
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Project description:Pattern-recognition receptor (PRR)-triggered immunity (PTI) plays a pivotal role in plant immunity to ward off a wide range of pathogenic microbes. The model liverwort Marchantia polymorpha is gaining popularity in investigating the evolution of plant-microbe interactions. The M. polymorpha is capable of triggering defense-related gene expression by sensing components in bacterial and fungal extracts, suggesting existence of PTI in this plant model. However, the molecular components that would form PTI in M. polymorpha have not yet been described. We show that, in M. polymorpha, lysin motif (LysM) receptor-like kinase (LYK) MpLYK1 and LYK-related (LYR) MpLYR, among four LysM receptor homologs, are required for sensing chitin and peptidoglycan (PGN) fragments and thereby triggering a series of immune responses. Phosphoproteomic analysis of M. polymorpha in response to chitin treatment comprehensively identified regulatory proteins that would shape LysM-mediated PTI. The identified proteins covered homologs of well-described PTI components in angiosperms as well as proteins whose roles in PTI are not yet determined including the blue-light receptor phototropin MpPHOT. We revealed that MpPHOT is required for a negative feedback of defense-related gene expression during PTI. Taken together, this study provides the basic framework of LysM-mediated PTI in M. polymorpha and demonstrates the utility of M. polymorpha as a plant model for discovering novel or fundamental molecular mechanisms underlying PRR-triggered immune signaling in plants.
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Project description:Expression analysis of Arabidopsis peptidoglycan (PGN) recognition mutants treated with PGN
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Project description:Individual acne comedones can undergo spontaneous remission in association with shrunken sebaceous glands (SGs) containing undifferentiated cells under unknown mechanisms. It is also still controversial whether sebum-induced follicular Propionibacterium acnes（P. acnes）interacts with the SGs. We explored the effects of P. acnes and peptidoglycan (PGN) on the aryl hydrocarbon receptor (AhR) activation, lipogenesis and differentiation in cultured human SZ95 sebocytes in vitro. Both formaldehyde-inactivated P. acnes and PGN upregulated mRNA levels of AhR charachteristic downstream genes CYP1A1, CYP1B1, CYP1A2, as well as significantly induced translocation of AhR protein from cytoplasm into nucleus. GSEA revealed pathways of downregulated lipogenesis and upregulated keratinization. In addition, P.acnes and PGN inhibited linoleic acid(LA)-induced neutral lipid synthesis and expressions of Keratin 7 and Mucin1/EMA (sebocyte markers) and increased the expression of Keratin 10 and involucrin (keratinocyte markers), which were abolished after AhR gene silencing. Moreover, inhibited expressions of lipogenesis-related genes such as SREBP1 were observed. In conclusion, we provide evidence that P. acnes can switch sebocytes into a keratinocyte-like differentiation with reduced lipogenesis via AhR, indicating that follicular P. acnes should not only be considered as acnegenic but also as a factor promoting acne remission through feedback regulation of sebum production.
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Project description:Bacteria and excessive inflammation are two main factors causing non-healing wounds. However, current studies have mainly focused on the inhibition of bacteria survival for wound healing while ignoring the excessive inflammation induced by dead bacteria-released lipopolysaccharide (LPS) or peptidoglycan (PGN). Herein, a boron-trapping strategy has been proposed to prevent both infection and excessive inflammation by synthesizing a class of reactive metal boride nanoparticles (MB NPs). Our results show that the MB NPs are gradually hydrolyzed to generate boron dihydroxy groups and metal cations while generating a local alkaline microenvironment. This microenvironment greatly enhances boron dihydroxy groups to trap LPS or PGN through an esterification reaction, which not only enhances metal cation-induced bacterial death but also inhibits dead bacteria-induced excessive inflammation both in vitro and in vivo, finally accelerating wound healing. Taken together, this boron-trapping strategy provides an approach to the treatment of bacterial infection and the accompanying inflammation.
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