Danger signals activate the innate immune system of a filamentous fungus during regeneration
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ABSTRACT:
PROVIDER: PRJNA476116 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7343320.fastq.gz | Fastqsanger.gz | |||
| SRR7343330.fastq.gz | Fastqsanger.gz | |||
| SRR7343340.fastq.gz | Fastqsanger.gz | |||
| SRR7343321.fastq.gz | Fastqsanger.gz | |||
| SRR7343331.fastq.gz | Fastqsanger.gz |
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Project description:The ability to respond to injury is a biological process conserved across kingdoms, which in some cases results in regeneration of an organism’s lost part or structure. Due to their immobility, multicellular fungi are prey to a variety of predators and are therefore constantly exposed to mechanical damage. Nevertheless, our current knowledge of how fungi respond to injury is scarce. Activation of injury responses and regeneration relies on the detection of danger or alarm signals known as Danger- or Damage-Associated Molecular Patterns. We show that Ca2+ influxes and extracellular ATP, two such signals, together with Mitogen-Activated Protein Kinases, play a key role in the control of hyphal regeneration in the filamentous fungus Trichoderma atroviride. We further show that these signaling cascades activate major transcriptional changes early after injury. We identified a set of regeneration genes related to cell signaling, stress responses, regulation of transcription, ribosome biogenesis/translation, replication and DNA repair. We uncovered the activation of an innate immune response, including HET domain genes, until now only known to participate in vegetative incompatibility. We show that fungal and animal regeneration share danger-signals, signaling cascades, and the activation of an immune system, challenging the current notion of the evolution of this process.
2018-08-14 | GSE115811 | GEO
Project description:The ability to respond to injury is a biological process shared by organisms of different kingdoms that can even result in complete regeneration of a part or structure that was lost. Due to their immobility, multicellular fungi are prey to various predators and are therefore constantly exposed to mechanical damage. Nevertheless, our current knowledge of how fungi respond to injury is scarce. Here we show that activation of injury responses and hyphal regeneration in the filamentous fungus Trichoderma atroviride relies on the detection of two danger or alarm signals. As an early response to injury, we detected a transient increase in cytosolic free calcium ([Ca2+]c) that was promoted by extracellular ATP, and which is likely regulated by a mechanism of calcium-induced calcium-release. In addition, we demonstrate that the mitogen activated protein kinase Tmk1 plays a key role in hyphal regeneration. Calcium- and Tmk1-mediated signaling cascades activated major transcriptional changes early following injury, including induction of a set of regeneration associated genes related to cell signaling, stress responses, transcription regulation, ribosome biogenesis/translation, replication and DNA repair. Interestingly, we uncovered the activation of a putative fungal innate immune response, including the involvement of HET domain genes, known to participate in programmed cell death. Our work shows that fungi and animals share danger-signals, signaling cascades, and the activation of the expression of genes related to immunity after injury, which are likely the result of convergent evolution.
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Project description:IL-10-Conditioned Dendritic Cells, Decommissioned for Recruitment of Adaptive Immunity, Elicit Innate Inflammatory Gene Products in Response to Danger Signals Dendritic cells (DCs) are the professional APCs of the immune system, enabling T cells to perceive and respond appropriately to potentially dangerous microbes, while also being able to maintain T cell tolerance toward self. In part, such tolerance can be determined by IL-10 released from certain types of regulatory T cells. IL-10 has previously been shown to render DCs unable to activate T cells and it has been assumed that this process represents a general block in maturation. Using serial analysis of gene expression, we show that IL-10 pretreatment of murine bone marrow-derived DCs alone causes significant changes in gene expression. Furthermore, these cells retain the ability to respond to Toll-like receptor agonists, but in a manner skewed toward the selective induction of mediators known to enhance local inflammation and innate immunity, among which we highlight a novel CXCR2 ligand, DC inflammatory protein-1. These data suggest that, while the presence of a protolerogenic and purportedly anti-inflammatory agent such as IL-10 precludes DCs from acquiring their potential as initiators of adaptive immunity, their ability to act as initiators of innate immunity in response to Toll-like receptor signaling is enhanced. Keywords: other
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Project description:Butyrate and propionate are microbial danger signals that activate the NLRP3-inflammasome in human macrophages in the presence of TLR stimulation
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Project description:Butyrate and propionate are microbial danger signals that activate the NLRP3-inflammasome in human macrophages in the presence of TLR stimulation
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Project description:Butyrate and propionate are microbial danger signals that activate the NLRP3-inflammasome in human macrophages in the presence of TLR stimulation
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Project description:Ca2+ is a second messenger that regulates a variety of cellular responses in fungi. However, the mechanism behind how Ca2+ signals are transmitted within the cell as they regulate downstream targets remains unclear. We used a fluorescent Ca2+ biosensor to visualize the changes in Ca2+ concentration in the hyphae of the filamentous fungus Aspergillus nidulans in response to thermal stress via infrared laser point irradiation, and then we analyzed the characteristics of the periodic Ca2+ influx in the hyphae. Stress-responsive Ca2+ pulses promoted the reorganization of the actin cytoskeleton and exocytosis, and they controlled the resumption, redirection, or branching of hyphal growth. To clarify how calcium signals are transmitted to downstream targets, we focused on calmodulin (CaM) and calcium/CaM-dependent protein kinases (CaMKs; CmkA, CmkB, and CmkC) by clarifying their localization and studying their interacting proteins by GFP-trap and MS analysis. Analysis of proteins that co-precipitated with CaM or CamKs showed that the calcium signaling pathway is involved in actin cytoskeleton rearrangement, vesicle transport, cell wall synthesis, and the cell wall integrity (CWI) pathway. Our approach enabled us to visualize the actual conduction of Ca2+ in hyphae in response to stress, and it clarified the downstream targets of CaM and CaMKs, thereby connecting the series of events, from input to output that are involved in calcium signaling.
2022-09-08 | PXD027777 | JPOST Repository
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Project description:Short chain fatty acids (SCFAs) are immunomodulatory compounds produced by the microbiome through fermentation of dietary fibre. Although they are generally considered beneficial for gut health, patients suffering from inflammatory bowel disease (IBD) have shown poor tolerance to fibre-rich diets, suggesting that SCFAs may have contrary effects under inflammatory conditions. To investigate this, we examined the effect of SCFAs on human macrophages in the presence of toll-like receptor agonists. In contrast to their anti-inflammatory effects under steady state conditions, we observed that the SCFAs butyrate and propionate triggered the activation of the NLRP3 inflammasome when added in conjunction with TLR agonists. Mechanistically, butyrate and propionate activated NLRP3 by inhibiting HDACs 1-3 and 10, leading to an uneven distribution of histone hyperacetylation that resulted in alterations in the transcriptome. Specifically, there was a lack of hyperacetylation at the loci of the CFLAR and IL10 genes, two important inhibitors of NLRP3 inflammasome activation. The concurrent loss of transcription and protein expression of cFLIP and IL-10 enabled caspase-8-dependent NLRP3-inflammasome activation. SCFA-driven NLRP3 activation did not require potassium efflux and did not result in cell death but rather triggered hyperactivation and IL-1b release. Our findings demonstrate that butyrate and propionate are bacterially-derived, viability-dependent danger signals (vita-PAMPs) that regulate NLRP3 inflammasome activation through epigenetic modulation of the inflammatory response.
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