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

ABSTRACT: 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.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE15762 | GEO | 2009/07/24

SECONDARY ACCESSION(S): PRJNA116795

REPOSITORIES: GEO

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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

mRNA-seq of wild-type(N2), hlh-11 knock-out(KO) and hlh-11 over-expression(OE) worms

Project description:Purpose: Comparing the transcriptome of wild-type(N2), hlh-11 knock-out and hlh-11 over-expression worms to identify genes with differential expression. Methods: For each condition, two replicates were examined. For each sample, approximately 2,000 synchronized young adult worms were collected and resuspended in TRIzon Reagent (CW0580, CWBIO). Total RNA was isolated by chloroform extraction, followed by isopropanol precipitation. Sequencing was performed using HiSeq2500. The clean reads were aligned to WBcel235 genomes with TopHat2. Gene differential expression was analyzed using DEseq2. A threshold of p < 0.05 was set to determine differentially expressed genes. Induction (KO_up or OE_up) or suppression (KO_down or OE_down) of genes were obtained through comparing gene expressions in hlh-11 KO or OE worms to wild-type N2. Results: >86% reads were uniquely mapped. 2637 genes were significantly up regulated and 2845 genes were significantly down regulated in hlh-11 knock-out worms compared to wild-type. 107 genes were significantly up regulated and 237 genes were significantly down regulated in hlh-11 over-expression worms compared to wild-type. Conclusions: This study revealed the genes transcriptionally regulated by hlh-11.

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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.

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

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A triple-HLH/bHLH Cascade Controls Cell Elongation Downstream of Multiple Hormonal and Environmental Signaling Pathways

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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

mRNA-seq of wild-type(N2), hlh-11 knock-out(KO) and hlh-11 over-expression(OE) worms

Project description:mRNA-seq of wild-type(N2), hlh-11 knock-out(KO) and hlh-11 over-expression(OE) worms

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Project description:The environmental and endogenous signals, light, temperature, brassinosteroid (BR), and gibberellin (GA), regulate cell elongation largely by controlling the expression of the PRE family helix-Loop-helix (HLH) factors, which promote cell elongation by interacting antagonistically with another HLH factor, IBH1. But the molecular mechanism by which PREs and IBH1 regulate gene expression has remained unknown. Here we show that IBH1 interacts with and inhibits a DNA-binding bHLH protein HBI1. Overexpression of HBI1 increased hypocotyl and petiole elongation, whereas dominant inactivation of HBI1 and its homologs caused a dwarf phenotype, indicating that HBI1 is a positive regulator of cell elongation. In vitro and in vivo experiments showed that HBI1 directly bound to the promoters and activated two EXPANSIN genes encoding cell wall-loosening enzymes; HBI1’s DNA-binding and transcriptional activities were inhibited by IBH1, but the inhibitory effects of IBH1 were abolished by PRE1. The results indicate that PREs activate the DNA-binding bHLH factor HBI1 by sequestering its inhibitor IBH1. Altering each of the three factors affected plant sensitivities to BR, GA, temperature, and light. Our study demonstrates that PREs, IBH1 and HBI1 form a chain of antagonistic switches that controls cell elongation downstream of multiple external and endogenous signals.

2015-01-01 | GSE41766 | GEO

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