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Caenorhabditis elegans

ABSTRACT: HLH-30/TFEB-mediated autophagy functions in a cell-autonomous manner for epithelium intrinsic cellular defense against bacterial pore-forming toxin in C. elegans

PROVIDER: PRJNA314272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3203635_1.fastq.gz	Fastqsanger.gz
	SRR3203635_2.fastq.gz	Fastqsanger.gz
	SRR3203636_1.fastq.gz	Fastqsanger.gz
	SRR3203636_2.fastq.gz	Fastqsanger.gz
	SRR3203637_1.fastq.gz	Fastqsanger.gz

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HLH-30/TFEB-mediated autophagy functions in a cell-autonomous manner for epithelium intrinsic cellular defense against bacterial pore-forming toxin in C. elegans

Project description:Autophagy is an evolutionarily conserved intracellular system that maintains cellular homeostasis by degrading and recycling damaged cellular components. The transcription factor HLH-30/TFEB-mediated autophagy has been reported to regulate tolerance to bacterial infection, but less is known about the bona fide bacterial effector that activates HLH-30 and autophagy. Here, we unveil that bacterial membrane pore-forming toxin (PFT) induces autophagy through an HLH-30-dependent manner in Caenorhabditis elegans. Moreover, autophagy controls the susceptibility of animals to PFT toxicity through xenophagic degradation of PFT and repair of membrane-pore cell-autonomously in the PFT-targeted intestinal cells in C. elegans. These results demonstrate that autophagic pathways and autophagy are induced partly at the transcriptional level through HLH-30 activation and are required to protect metazoan upon PFT intoxication. Together, our data show a new and powerful connection between HLH-30-mediated autophagy and epithelium intrinsic cellular defense against the single most common mode of bacterial attack in vivo.

2016-11-01 | GSE78878 | GEO

HLH-30/TFEB-regulated autophagy mediates sexual dimorphism in immunity in Caenorhabditis elegans

Project description:Sexual dimorphism affects diverse biological functions such as immune responses. However, mechanisms by which different sexes alter immunity remained largely unknown. By using Caenorhabditis elegans as a model, here we show that male animals exhibit enhanced immunity against various pathogenic bacteria via upregulating autophagy. We found that male C. elegans displayed upregulation of helix loop helix 30 (HLH-30)/transcription factor EB (TFEB), a transcription factor crucial for autophagy, which contributed to the enhanced anti-bacterial immunity. We showed that autophagy-related protein 2 (atg-2) that is upregulated by HLH-30/TFEB, mediated increased immunity in male animals. Thus, male C. elegans appear to be equipped with enhanced autophagy for increasing pathogen resistance, likely conferring prolonged mate search with less infection.

2024-08-22 | GSE245430 | GEO

A conserved cysteine-based redox mechanism sustains TFEB/HLH-30 activity under persistent stress

Project description:Mammalian TFEB and TFE3, as well as their ortholog in C. elegans HLH-30, play an important role in mediating cellular response to a variety of stress conditions, including nutrient deprivation, oxidative stress and pathogen infection. In this study we identify a novel mechanism of TFEB/HLH-30 regulation through a cysteine-mediated redox switch. Under stress conditions, TFEB-C212 undergoes oxidation, allowing the formation of intermolecular disulfide bonds that result in TFEB oligomerization. TFEB oligomers display increased resistance to mTORC1-mediated inactivation and are more stable under prolonged stress conditions. Mutation of the only cysteine residue present in HLH-30 (C284) significantly reduced its activity, resulting in developmental defects and increased pathogen susceptibility. Therefore, cysteine oxidation represents a new type of TFEB post-translational modification that functions as a molecular switch to link changes in redox balance with expression of TFEB/HLH-30 target genes.

2021-01-22 | PXD022258 | Pride

YAP promotes cell-autonomous immune responses in vitro to tackle intra-cellular Staphylococcus aureus

Project description:Transcriptional cofactors YAP/TAZ have recently been found to support autophagy and inflammation, which are part of cell autonomous immunity and are critical in antibacterial defense. Here, we studied the role of YAP against Staphylococcus aureus using CRISPR/Cas9-mutated HEK293 cells and a primary cell-based organoid model. We found that S. aureus infection increases YAP transcriptional activity, which is required to reduce intracellular S. aureus replication. A 770-gene targeted transcriptomic analysis revealed that YAP upregulates genes involved in autophagy/lysosome and inflammation pathways in both infected and uninfected conditions. The YAP/TEAD transcriptional activity promotes autophagic flux and lysosomal acidification, which are important for defense against intracellular S. aureus. Furthermore, the staphylococcal toxin C3 exoenzyme EDIN-B was found effective in preventing YAP-mediated cell-autonomous immune response. This study provides new insights on the anti-S. aureus activity of YAP, which could be conserved for defense against other intracellular bacteria.

2022-05-03 | GSE197181 | GEO

Glycerol 3-phosphate phosphatase/PGPH-2 counters metabolic stress and promotes healthy aging via a glycogen sensing-AMPK-HLH-30-autophagy axis in C. elegans

Project description:Metabolic stress caused by excess nutrients accelerates aging. We recently demonstrated that the newly discovered enzyme glycerol-3-phosphate phosphatase (G3PP; gene Pgp), which operates an evolutionarily conserved glycerol shunt that hydrolyzes glucose-derived glycerol-3-phosphate to glycerol, counters metabolic stress and promotes healthy aging in C. elegans. However, the mechanism whereby G3PP activation extends healthspan and lifespan, particularly under glucotoxicity, remained unknown. Here, we show that the overexpression of the C. elegans G3PP homolog, PGPH-2, decreases fat levels and mimics, in part, the beneficial effects of calorie restriction, particularly in glucotoxicity conditions, without reducing food intake. PGPH-2 overexpression depletes glycogen stores activating AMP-activate protein kinase, which leads to the HLH-30 nuclear translocation and activation of autophagy, promoting healthy aging. Transcriptomics reveal an HLH-30-dependent longevity and catabolic gene expression signature with PGPH-2 overexpression. Thus, G3PP overexpression activates three key longevity factors, AMPK, the TFEB homolog HLH-30, and autophagy, and may be an attractive target for age-related metabolic disorders linked to excess nutrients.

2024-02-07 | MTBLS6847 | MetaboLights

Mass spectrometry-based characterization of secretomes from different strains of Pseudomonas chlororaphis and Pseudomonas entomophila.

Project description:To characterize the molecular basis of cytotoxicity of different Pseudomonas species and strains, we analyzed the protein content of secretomes of three P. chlororaphis strains (CIP63, CIP75 and the reference strain PA23) and of six P. entomophila strains (L48 WT, or deleted for various virulence factors: the global activator GacA, the pore-forming toxin Mnl, the pore-forming toxin ExlA, and double mutants for these genes).

2022-07-25 | PXD029397 | Pride

Transcriptional regulation of the innate immune reponse by the MITF/TFE3 family

Project description:To understand the activation of the MITF/TFE transcription factors in effective defense against pathogens we examined the genome wide distribution of TFE3 in control and activated mouse macrophages. It was determined that TFEB and TFE3 collaborate with each other to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of proinflammatory cytokines and key mediators of the inflammatory response. 4 samples were analyzed: Background Control, Control, Starvation, LPS

2016-02-01 | E-GEOD-75822 | biostudies-arrayexpress

RNA seq to determine differential gene expression in pgph-2 oe C.elegans animals and the subset of HLH-30-dependent genes on normal growth and excess glucose conditions.

Project description:Metabolic stress caused by excess nutrients accelerates aging. We recently demonstrated that the newly-discovered enzyme glycerol-3-phosphate phosphatase (G3PP; gene Pgp), which operates an evolutionarily conserved glycerol shunt that hydrolyzes glucose-derived glycerol-3-phosphate to glycerol, counters metabolic stress and promotes healthy aging in C. elegans. However, the mechanism whereby G3PP activation extends healthspan and lifespan, particularly under glucotoxicity, remained unknown. We demonstrated that G3PP (PGPH-2) overexpression activates three key longevity factors, AMPK, the TFEB homolog HLH-30, and autophagy, and is an attractive target for age-related metabolic disorders linked to excess nutrients. This transcriptomics analysis was designed to determine genes that are differentially regulated in pgph-2 oe animals in comparison to wild-type animals on normal and excess glucose conditions. To determine the role of HLH-30 in the regulation of gene expression, we also used pgph-2 oe; hlh-30 and hlh-30 mutant animals and found a signature mediated by pgph-2 oe and HLH-30-dependent.

2023-04-30 | GSE228784 | GEO

HLH-30/TFEB is a master regulator of reproductive quiescence

Project description:All animals have evolved the ability to survive nutrient deprivation, and nutrient signaling pathways are conserved modulators of health and disease. In C. elegans, late-larval starvation provokes adult reproductive diapause (ARD), a long-lived quiescent state that enables animals to survive months without food, yet underlying molecular mechanisms remain unknown. Here, we show that ARD is distinct from other forms of diapause, and shows surprisingly little requirement for canonical longevity pathways, autophagy and fat metabolism. Instead ARD depends dramatically on HLH-30/TFEB transcription factor to promote morphologic and metabolic remodeling involved in ARD entry, survival, and recovery, suggesting it is a master regulator of reproductive quiescence. TFEB transcriptome and genetic analyses reveal that Max-like HLH factors, mTOR, AMP-kinase, protein synthesis, and mitochondrial fusion are target processes that promote ARD longevity. Evidently reproductive quiescence rewires metabolism in unique ways to ensure long-term survival, and could illuminate similar mechanisms acting in latent tumorigenesis, and long-term fasting.

2020-03-30 | GSE126632 | GEO

HLH-30/TFEB-regulated autophagy mediates sexual dimorphism in immunity in Caenorhabditis elegans

Project description:HLH-30/TFEB-regulated autophagy mediates sexual dimorphism in immunity in Caenorhabditis elegans

| PRJNA1028495 | ENA