The Arabidopsis homolog of human G3BP1 is a key regulator of stomatal and aploplastic immunity
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE107786 | GEO | 2018/06/01
REPOSITORIES: GEO
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Project description:The Arabidopsis homolog of human G3BP1 is a key regulator of stomatal and aploplastic immunity
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Project description:A multibillion dollar pharmaceutical industry targets purinergic signaling pathways in humans. However, in contrast, little is known about purinergic signaling in plants. Extracellular adenosine-5’-triphosphate (eATP) acts as a damage-associated molecular pattern (DAMP) in both animals and plants. The first plant eATP receptor, DORN1, was identified in Arabidopsis, defining a new kinase family (P2K) of purinoceptors. Stomates are leaf pores that control gas exchange and, therefore, impact critical functions such as photosynthesis and drought tolerance. Stomates are also the prefer entry point for leaf pathogens. The addition of ATP led to the rapid closure of Arabidopsis leaf stomates resulting in enhanced resistance to the bacterial pathogen Psuedomonas syringae. The data indicate that this response is mediated by eATP recognition by DORN1 followed by direct phosphorylation of the NADPH oxidase RBOHD, resulting in elevated production of reactive oxygen species and stomatal closure. Mutation of the DORN1 phosphorylation sites on RBOHD eliminated the ability of eATP to induce stomatal closure. To date, in contrast to work in animals, purinergic signaling in plants has been viewed as a curiosity without any direct, mechanistic connection to key plant processes. The data presented clearly demonstrates eATP as an important signal controlling stomatal aperture with important implications for the control of plant photosynthesis, water homeostasis, pathogen resistance and ultimately yield.
2018-10-24 | PXD006678 | Pride
Project description:Stomata in the plant epidermis play a vital role in growth and survival by controlling gas exchange and immunity to pathogens. A genetic frame of key transcriptional factors and cellular communication has been established, by which plants modulate stomatal cell fate and patterning. miRNAs contribute to functional and developmental plasticity in multicellular organisms. However, it remains very elusive as to whether miRNAs pitch in stomatal development. Here, we reveal dynamic miRNA expression profiles from stomatal lineage cells in a development stage-specific manner and show that stomatal lineage miRNAs positively and negatively regulate stomatal formation and pattern to avoid clustered and paired stomata. Target prediction of stomatal lineage miRNAs suggests potential cellular processes involved in stomatal development. Furthermore, dysregulation of stomatal lineage miRNAs and their target mRNAs disclose unexpected genetic pathways modulating stomatal development. Our study demonstrates that miRNAs constitute an additional layer in the complex regulatory mechanism of stomatal development.
2020-02-03 | GSE140918 | GEO
Project description:Systemic Acquired Resistance (SAR) as a plant immune response improves immunity of distal tissue after local exposure to a pathogen. Stomata pores on leaf surfaces are formed by guard cells that recognize bacterial pathogens via pattern recognition receptors. We found that Arabidopsis thaliana plants that have been previously exposed to the pathogenic bacteria Pseudomonas syringae pv. tomato DC3000 (Pst) exhibit an altered stomatal response compared to control plants when systemic leaves are later exposed to the bacteria. Reduced stomatal apertures of SAR primed plants lead to decreases in the number of bacteria that enter the apoplastic space of the leaves. To examine how SAR affects molecular processes in guard cells of distal leaves, we collected Arabidopsis guard cell samples and extracted lipids, metabolites and proteins using a 3-in-1 method. Multi-omic results have revealed molecular components of SAR response specific to the functions of guard cells and roles of ROS and fatty acid signaling in guard cell SAR response. Additionally, our results show an increase in palmitic acid and its derivative 9-PAHSA in primed guard cells. Palmitic acid may play a role as an agonist to Flagellin Sensitive 2 (FLS2), which initiates stomatal closure upon perception of bacterial flagella. The improved understanding of how SAR immune signals affect stomatal movement and immunity can aid biotechnology and marker-based breeding of crops for enhanced disease resistance.
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Project description:we identify G3BP1 as a novel rG4-binding protein, and reveal that G3BP1 can modulate mRNA stability through its binding with rG4 structures
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Project description:To investigate whether G3BP1 binds to telomeric DNA, we performed the ChIP-seq analysis of G3BP1 in KGN cells.
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Project description:Melanoma is the leading cause of skin cancer-related deaths, and current melanoma therapies, including targeted therapies and immunotherapies, benefit only a subset of metastatic melanoma patients due to either intrinsic or acquired resistance. LIM domain kinase 2 (LIMK2) is a serine/threonine kinase that plays an important role in the regulation of actin filament dynamics. Here, we show that LIMK2 is overexpressed in melanoma, and its genetic or pharmacological inhibition impairs melanoma tumor growth and metastasis in both cell culture and mice. To determine the mechanism by which LIMK2 promotes melanoma tumor growth and metastatic progression, we performed a phosphoproteomics analysis and identified G3BP1 as a key LIMK2 target, which mirrored the effects of LIMK2 inhibition when inhibited. To further determine the role of G3BP1 downstream of LIMK2, we knocked down the expression of G3BP1, performed RNA-seq analysis, and identified ESM1 as a downstream target of G3BP1. G3BP1 was required for ESM1 mRNA stability, and ESM1 ectopic expression rescued LIMK2 or G3BP1 inhibition-induced suppression of melanoma growth and metastatic attributes. These results collectively identify the LIMK2→G3BP1→ESM1 pathway as a facilitator of melanoma tumor growth and metastasis and document that LIMK2 is a therapeutically tractable target for melanoma therapy.
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Project description:Plants are exposed to regular diurnal rhythms of light and dark. Changes in the photoperiod by the prolongation of the light period cause photoperiod stress in short day-adapted Arabidopsis thaliana. Here we report on the transcriptional response to photoperiod stress of wild-type A. thaliana and photoperiod stress-sensitive cytokinin signaling and clock mutants. Transcriptomic changes induced by photoperiod stress included numerous changes in reactive oxygen species (ROS)-related transcripts and showed a strong overlap with alterations occurring in response to ozone stress and pathogen attack, which have in common the induction of an apoplastic oxidative burst. A core set of photoperiod stress-responsive genes has been identified, including salicylic acid (SA)-biosynthesis and -signaling genes. Genetic analysis revealed a central role for NPR1 in the photoperiod stress response as npr1-1 mutants were stress-insensitive. Photoperiod stress treatment led to a strong increase in camalexin levels which is also observed in response to pathogen infections. Photoperiod stress induced the resistance of Arabidopsis plants to a subsequent infection by Pseudomonas syringae pv. tomato DC3000 indicating priming of the defence response. Together, photoperiod stress causes transcriptional reprogramming resembling plant pathogen defence responses and induces systemic acquired resistance in the absence of a pathogen.
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Project description:Speckle-type POZ protein (SPOP), an E3 ubiquitin ligase, acts as a tumor suppressor. We identified G3BP1 as non-substrate interactor of SPOP. G3BP1 is a well-known oncogene in many cancer types, but its role in prostate cancer (PCa) remains largely elusive. We showed that G3BP1 functions as an upstream regulator and potent endogenous inhibitor of Cul3SPOP, suggesting a distinctive Cul3SPOP inactivation independent of SPOP mutations. Transcriptomic analysis together with functional studies revealed that the G3BP1-SPOP ubiquitin signaling axis is involved in PCa progression through activating AR signaling. Further, AR upregulates G3BP1 to potentiate feed-forward amplification of signaling through G3BP1-SPOP axis. Overall, we show G3BP1high PCa tumors constitute a new subset where G3BP1 inhibits Cul3SPOP function to upregulate AR signaling, and promotes tumorigenesis.
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Project description:Regulation of Stomatal Development by Stomatal Lineage miRNAs
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