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Simple Nutrients Bypass the Requirement for HLH-30 in Coupling Lysosomal Nutrient Sensing to Survival.

ABSTRACT: In this study, we subjected worms deficient in HLH-30, a master regulator of lysosome biogenesis, to starvation followed by refeding various food sources and analyzed their transcriptional profiles.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE126061 | GEO | 2019/05/14

REPOSITORIES: GEO

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Simple nutrients bypass the requirement for HLH-30 in coupling lysosomal nutrient sensing to survival.

Project description: Not available

| S-EPMC6516633 | biostudies-literature

Simple Nutrients Bypass the Requirement for HLH-30 in Coupling Lysosomal Nutrient Sensing to Survival.

Project description:Simple Nutrients Bypass the Requirement for HLH-30 in Coupling Lysosomal Nutrient Sensing to Survival.

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A cascade for zinc mediated transcriptional activation by the zinc-sensing nuclear receptor HIZR-1 on the regulator of lysosome biogenesis HLH-30 to achieve homeostasis

Project description:Zinc is an essential element for animals and stored in de novo synthesized lysosome related organelles called bilobed granules in Caenorhabditis elegans. Defining how zinc regulated transcription drives the observed lysosome remodeling is key to understand zinc homeostasis processes. Here we describe a positively regulated zinc network controlled by HIZR-1 and HLH-30, the zinc sensor and the master regulator of the autophagy-lysosomal pathway in Caenorhabditis elegans, respectively; essential for connecting zinc homeostasis to lysosome biogenesis. Our studies indicate that either hizr-1 and hlh-30 are necessary and sufficient to activate transcription of lysosome-genes under high dietary zinc conditions. Consistent with the hizr-1 and hlh-30 dependency for high zinc response, we found DNA enhancer elements corresponding to the high zinc activation element consistently adjacent to E-boxes in the promoter regions of lysosome-genes. We defined a regulatory network based on the contribution of each transcription factor. Since zinc cannot be degraded, the autophagy-lysosomal pathway could play a key role in removing zinc excess

2021-05-15 | GSE172079 | 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

Transcription profiling of C. elegans wild type (N2) and hlh-30(tm1978) mutants

Project description:The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor. Experiment Overall Design: Total RNA from three biological replicates were isolated from embryos, L1 larvae, and L2 larvae from both wild type and hlh-30(tm1978) mutant worms

2009-08-07 | E-GEOD-15762 | biostudies-arrayexpress

Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms

2009-07-24 | GSE15762 | GEO

PRMT-7/PRMT7 activates HLH-30/TFEB to guard plasma membrane integrity compromised by pore-forming toxins

Project description:This research reveals that protein arginine methyltransferase-7 (PRMT-7) is indispensable to the nuclear transactivation of HLH-30. We demonstrated that PRMT-7 participates in the methylation of HLH-30 on its Rag complex binding domain to facilitate its nuclear localization. Moreover, we showed that PRMT7 is evolutionarily conserved to regulate TFEB cellular localization and repair plasma damage caused by PFTs in human intestinal cells.

2024-01-26 | PXD043101 | Pride

Neuronal HLH-30 regulates glp-1 longevity independent of neuronal MML-1/MXL-2

Project description:Accumulating evidence has demonstrated the presence of inter-tissue communication regulating systemic aging, but the underlying molecular network has not been fully explored. We and others previously showed that two basic helix-loop-helix transcription factors, MML-1 and HLH-30, are required for lifespan extension in several longevity paradigms, including germline-less Caenorhabditis elegans. However, it is unknown what tissues these factors target to promote longevity. Here, using tissue-specific knockdown experiments, we found that MML-1 and its heterodimer partners MXL-2 and HLH-30 act primarily in neurons to extend longevity in germline-less animals. Neuronal functions of MML-1/MXL-2 and HLH-30 are also essential to prevent aging in non-neuronal tissues, including muscle and the intestine. Interestingly, however, both the temporal requirement and the downstream function of MML-1 in neurons were distinct from those of HLH-30. MML-1 was active early, while HLH-30 functioned later in life to sustain longevity in germline-less animals. Moreover, neuronal RNA interference (RNAi)-based transcriptome analysis revealed that the glutamate transporter GLT-5 is a novel downstream target of MML-1 but not HLH-30. Furthermore, the MML-1–GTL-5 axis in neurons is critical to prevent an age-dependent collapse of proteostasis and increased oxidative stress through autophagy and peroxidase MLT-7, respectively, in long-lived animals. Collectively, our study revealed that systemic aging is regulated by a novel molecular network involving neuronal MML-1 function in both neural and peripheral tissues.

2023-09-18 | GSE234429 | GEO

Neuronal HLH-30/TFEB modulates muscle mitochondrial fragmentation to improve thermoresistance in C. elegans

Project description:RNA-seq performed for studying transcriptomic changesmodulated by neuronal HLH-30 during heat stress

2022-12-31 | GSE200383 | 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

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