Hcf-1(-) transcriptional profiling
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE30725 | GEO | 2011/07/23
SECONDARY ACCESSION(S): PRJNA144389
REPOSITORIES: GEO
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Project description:We used microarrays to identify genes regulated by HCF-1 in a daf-16-dependent manner. Samples from young adult worms were hybridized to Agilent microarrays to identify genes differentially expressed in hcf-1(pk924)/daf-16(mgDf47);hcf-1(pk924) and compared to hcf-1(pk924)/N2 arrays.
2011-07-22 | E-GEOD-30725 | biostudies-arrayexpress
Project description:To identify DAF-16-dependent transcriptional alterations that occur in a long-lived C. elegans strain, we used cDNA microarrays and genomic analysis to identify putative direct and indirect DAF-16 transcriptional target genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-08-10 | GSE3089 | GEO
Project description:The insulin-like signaling (ILS) pathway regulates metabolism and is known to modulate adult lifespan in C. elegans. Altered stress responses and resistance to a wide range of stressors are also associated with changes in ILS and contribute to enhanced longevity. The transcription factors DAF-16 and HSF-1 are key effectors of the longevity phenotype. We demonstrate that increased intrinsic thermotolerance, due to lower ILS, is not dependent on stress induced HSF-1 transcriptional responses but instead requires active protein translation. Translation profiling experiments reveal genes that are post-transcriptionally regulated in response to altered ILS during heat shock in a DAF-16-dependent manner. Furthermore, several novel proteins are specifically required for ILS effects on thermotolerance. We propose that lowered-ILS results in DAF-16-induced metabolic and physiological changes that precondition a translational response to modulated survival under acute stress.
2010-06-17 | GSE22383 | GEO
Project description:Here we study the effect of doxycycline induced expression of HCF-2 (the host-cell-factor 2) proteins - HCF-2WT and its mutant HCF-2Fn3nc* on the global gene expression in HEK-293 cells. We identified 7175 genes that were differentially expressed after day 1 in any of the HCF-2WT or HCF-2Fn3nc* samples (log2 (fold change) > 0.5 or < -0.5 and FDR < 0.05). The maximal gene-expression changes over time were on day 6 in each case, with more genes up-regulated (2199 vs. 1241) in the HCF-2WT samples and more genes down-regulated (2513 vs. 1555) in the HCF-2Fn3nc* samples after six days compared to day 1. Notably, there was little overlap between the genes affected by the induced synthesis of HCF-2WT or HCF-2Fn3nc* indicating that the HCF-2Fn3nc* mutation seriously disrupts HCF-2 function. In total, we found that up-regulated genes in HCF-2WT were associated with developmental and morphogenesis programs induction, whereas down-regulated genes were linked to the inhibition of cellular metabolism and proliferation.
2019-04-17 | GSE128076 | GEO
Project description:The insulin-like signaling (ILS) pathway regulates metabolism and is known to modulate adult lifespan in C. elegans. Altered stress responses and resistance to a wide range of stressors are also associated with changes in ILS and contribute to enhanced longevity. The transcription factors DAF-16 and HSF-1 are key effectors of the longevity phenotype. We demonstrate that increased intrinsic thermotolerance, due to lower ILS, is not dependent on stress induced HSF-1 transcriptional responses but instead requires active protein translation. Translation profiling experiments reveal genes that are post-transcriptionally regulated in response to altered ILS during heat shock in a DAF-16-dependent manner. Furthermore, several novel proteins are specifically required for ILS effects on thermotolerance. We propose that lowered-ILS results in DAF-16-induced metabolic and physiological changes that precondition a translational response to modulated survival under acute stress. 72 experimental samples were analyzed using custom oligo microarrays. A wild type sample pool was used as the Cy3 reference/control for all experimetal samples. All extracted RNA prior to array analysis was fractioned (via a sucrose gradient) based on ribosomal loading and pooled into ribosomal and free RNA (F1), light polysomes (F2) and heavy polysomes (F3) as described in the experimental procedures. The control RNAi is ‘empty’ vector L4440 RNAi feeding vector plasmid (1999 Firelab vector kit) transformed HT115(DE3), which was obtained from the Caenorhabditis Genetics Center (University of Wisconsin).
2010-06-17 | E-GEOD-22383 | biostudies-arrayexpress
Project description:Coordinated regulation of stress response pathways is crucial for cellular homeostasis. However, crosstalk between the different stress pathways and the physiological significance of this crosstalk remain poorly understood. In this study, using the model organism C. elegans, we discovered that suppression of the transcription factor LET-607/CREBH, a regulator of cellular defense and proteostatic responses, triggers adaptive induction of DAF-16-dependent stress responses. Suppression of LET-607 improves stress resistance and extends C. elegans lifespan in a DAF-16-dependent manner. We identified the sphingomyelin synthase SMS-5 to be a central mediator in the communication between LET-607 and DAF-16. SMS-5 reduces the contents of unsaturated phosphatidylcholine (PC), which activates DAF-16 through ITR-1-dependent calcium signaling and calcium-sensitive kinase PKC-2. Our data reveal the significance of crosstalk between different stress pathways in animal fitness and identify LET-607/CREBH and specific PC as regulators of DAF-16 and longevity.
2021-05-05 | GSE155935 | GEO
Project description:We confirmed that the life span of C. elegans feeding hns mutant E. coli was increased. hns mutant E. coli was found to regulate lifespan of C. elegans through daf-16 activation in C. elegans. It is well known that daf-16 is the transcription factor of the insulin/IGF-1 signaling pathway and it is known to regulate downstream genes such as longevity, stress response, and dauer diapause regulation genes. Thus, we performed Next Generation Sequencing(NGS) to investigate the downstream genes regulated by daf-16 in C. elegans that are activated by hns mutant E. coli. N2 wild type worms and daf-16 mutant worms were fed with BW25113 wild type E. coli and hns mutant E. coli, respectively, and then NGS was performed by harvesting the worms and purifying the RNA. We investigated how the downstream genes of daf-16 of C. elegans, which is regulated by hns mutant E. coli, differs from the downstream genes of daf-16 of C. elegans, which is regulated by the insulin/IGF-1 signaling pathway. To do this, we carried out the analysis including two previous studied papers that analyzed the daf-16 downstream genes related to the insulin/IGF-1 signaling pathway. Surprisingly, only 6 genes were up-regulated in all three experiments and 288 genes were found to be dependent on daf-16 and hns mutant E. coli. This study indicated that hns mutant E. coli regulate daf-16 distinct from insulin/IGF-1 signaling pathway on C. elegans.
2020-07-29 | GSE114160 | GEO
Project description:We identified genes inversely regulated by pmk-1 null mutation and pmk-1(D327E). We also identified genes working through daf-16, working around daf-16 and working independent of daf-16
2022-07-12 | GSE192941 | GEO
Project description:Background and Aims: Host-cell factor 1 (HCF-1), encoded by the ubiquitously expressed X linked gene Hcfc1, is an epigenetic co-regulator important for mouse development and cell proliferation, including during liver regeneration. Here, we examine the role of HCF-1 in adult tissue physiology using, as model, the resting mouse liver. Methods: We used a hepatocyte-specific inducible Hcfc1 knock-out allele (called Hcfc1hepKO), to induce HCF-1 loss in hepatocytes of hemizygous Hcfc1 hepKO/Y males by four days. In heterozygous Hcfc1hepKO/+ females, owing to random X-chromosome inactivation, upon Hcfc1hepKO allele induction, a 50/50 mix of HCF-1 positive and negative hepatocyte clusters is engineered. Results: The livers with Hcfc1hepKO/Y hepatocytes displayed a 21–24-day terminal non-alcoholic fatty liver (NAFL) followed by non-alcoholic steatohepatitis (NASH) disease progression typical of severe NAFL disease (NAFLD). In contrast, in livers with heterozygous Hcfc1hepKO/+ hepatocytes, HCF-1-positive hepatocytes replaced HCF-1-negative hepatocytes and revealed only mild-NAFL development. Loss of HCF-1 led to loss of PGC1 alpha protein levels, probably owing to its destabilization, and deregulation of gene expression particularly of genes involved in mitochondrial structure and function, likely explaining the severe Hcfc1hepKO/Y liver pathology. Interestingly, although HCF-1 binds to over 5000 transcriptional start sites in the resting liver, expression of only a minor subset of the associated genes was affected by HCF-1 loss. Conclusion: HCF-1 is essential for proper liver physiology likely playing both transcriptional and non-transcriptional roles. These genetically-engineered loss-of-HCF-1 mice represent models for the study of NASH and NAFLD resolution.
2019-02-27 | GSE115766 | GEO
Project description:Background and Aims: Host-cell factor 1 (HCF-1), encoded by the ubiquitously expressed X linked gene Hcfc1, is an epigenetic co-regulator important for mouse development and cell proliferation, including during liver regeneration. Here, we examine the role of HCF-1 in adult tissue physiology using, as model, the resting mouse liver. Methods: We used a hepatocyte-specific inducible Hcfc1 knock-out allele (called Hcfc1hepKO), to induce HCF-1 loss in hepatocytes of hemizygous Hcfc1 hepKO/Y males by four days. In heterozygous Hcfc1hepKO/+ females, owing to random X-chromosome inactivation, upon Hcfc1hepKO allele induction, a 50/50 mix of HCF-1 positive and negative hepatocyte clusters is engineered. Results: The livers with Hcfc1hepKO/Y hepatocytes displayed a 21 24-day terminal non-alcoholic fatty liver (NAFL) followed by non-alcoholic steatohepatitis (NASH) disease progression typical of severe NAFL disease (NAFLD). In contrast, in livers with heterozygous Hcfc1hepKO/+ hepatocytes, HCF-1-positive hepatocytes replaced HCF-1-negative hepatocytes and revealed only mild-NAFL development. Loss of HCF-1 led to loss of PGC1 alpha protein levels, probably owing to its destabilization, and deregulation of gene expression particularly of genes involved in mitochondrial structure and function, likely explaining the severe Hcfc1hepKO/Y liver pathology. Interestingly, although HCF-1 binds to over 5000 transcriptional start sites in the resting liver, expression of only a minor subset of the associated genes was affected by HCF-1 loss. Conclusion: HCF-1 is essential for proper liver physiology likely playing both transcriptional and non-transcriptional roles. These genetically-engineered loss-of-HCF-1 mice represent models for the study of NASH and NAFLD resolution.
2019-02-27 | GSE115767 | GEO