Genome-wide identification of DAF-12 binding sites in Caenorhabditis elegans
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE28350 | GEO | 2011/04/05
SECONDARY ACCESSION(S): PRJNA139461
REPOSITORIES: GEO
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Project description:Under adverse environmental conditions, nematodes arrest into dauer, an alternative developmental stage for diapause. Dauers endure unfavorable environment and interact with host animals to access favorable environments, thus playing a critical role in the survival of both free-living and parasitic nematodes. Here, we discovered that in Caenorhabditis elegans, daf-42 is essential for development into dauer stage, as the null mutant shows lethal phenotype during dauer entry. To examine the transcriptional changes accompanied by the absence of DAF-42 during dauer entry, we performed RNA-sequencing on daf-2 and daf-2; daf-42 worms at 52 hours after egg laying (HAE) and 60 HAE, the time at which 0% and about 40% of daf-2; daf-42 mutants form dead dauer at 25 degrees Celcius, respectively. daf-2 control worms develop into dauer stage after 60 HAE, and half of its population develop into dauer by 72 HAE, when raised at 25 degrees Celcius.
2023-04-23 | GSE230353 | GEO
Project description:Many tissue-specific stem cells maintain the ability to produce multiple cell types during long periods of non-division, or quiescence. FOXO transcription factors promote quiescence and stem cell maintenance, but the mechanisms by which FOXO proteins promote multipotency during quiescence are still emerging. The single FOXO ortholog in C. elegans, daf-16, promotes entry into a quiescent and stress-resistant larval stage called dauer in response to adverse environmental cues. During dauer, stem and progenitor cells maintain or re-establish multipotency to allow normal development to resume after dauer. We find that during dauer, daf-16/FOXO prevents epidermal stem cells (seam cells) from prematurely adopting differentiated, adult characteristics. In particular, dauer larvae that lack daf-16 misexpress collagens that are normally adult-enriched. Using col-19p::gfp as an adult cell fate marker, we find that all major daf-16 isoforms contribute to opposing col-19p::gfp expression during dauer. By contrast, daf-16(0) larvae that undergo non-dauer development do not misexpress col-19p::gfp. Adult cell fate and the timing of col-19p::gfp expression are regulated by the heterochronic gene network, including lin-41 and lin-29. lin-41 encodes an RNA-binding protein orthologous to LIN41/TRIM71 in mammals, and lin-29 encodes a conserved zinc finger transcription factor. In non-dauer development lin-41 opposes adult cell fate by inhibiting the translation of lin-29, which directly activates col-19 transcription and promotes adult cell fate. We find that during dauer, lin-41 blocks col-19p::gfp expression, but surprisingly, lin-29 is not required in this context. Additionally, daf-16 promotes the expression of lin-41 in dauer larvae. The col-19p::gfp misexpression phenotype observed in dauer larvae with reduced daf-16 requires the downregulation of lin-41, but does not require lin-29. Taken together, this work demonstrates a novel role for daf-16/FOXO as a heterochronic gene that promotes expression of lin-41/TRIM71 to contribute to multipotent cell fate in a quiescent stem cell model.
2021-10-09 | GSE179166 | GEO
Project description:Transcriptional profiling of whole day 1 adult C. elegans, comparing animals carrying the m79 mutation in the daf-10 gene and wild-type isogenic animals. Genes that act downstream of sensory neurons to influence longevity, dauer formation and pathogen responses in Caenorhabditis elegans Manuscript abstract: Two-condition experiments, daf-10 vs wt, 3 biological repeats of each grown in parallel, verified lifespan increase in daf-10 mutant animals
2012-11-01 | E-GEOD-41943 | biostudies-arrayexpress
Project description:Transcriptional profiling of whole day 1 adult C. elegans, comparing animals carrying the m79 mutation in the daf-10 gene and wild-type isogenic animals. Genes that act downstream of sensory neurons to influence longevity, dauer formation and pathogen responses in Caenorhabditis elegans Manuscript abstract:
2012-11-01 | GSE41943 | GEO
Project description:RNA-seq profile of two daf-2 (e1370);daf-12(m20) samples
2019-12-03 | GSE68669 | GEO
Project description:Post-embryonic development of the nematode C. elegans is governed by nutrient availability. L1-stage larvae remain in a state of developmental arrest after hatching until they feed. This “L1 arrest” (or "L1 diapause") is associated with increased stress resistance, supporting starvation survival. Loss of the transcription factor daf-16/FOXO, an effector of insulin/IGF signaling, results in arrest-defective and starvation-sensitive phenotypes. We show that daf-16/FOXO regulates L1 arrest cell-nonautonomously, suggesting that insulin/IGF signaling regulates at least one additional signaling pathway. We used mRNA-seq to identify candidate signaling molecules affected by daf-16/FOXO during L1 arrest. daf-16/FOXO had overlapping but distinct effects on gene expression in L1 arrest compared to daf-2/InsR adults. Notably, dbl-1/TGF-β, a ligand for the Sma/Mab pathway, and daf-36, which encodes an upstream component of the daf-12/NHR steroid hormone signaling pathway, were up-regulated during L1 arrest in a daf-16/FOXO mutant. Using genetic epistasis analysis, we show that dbl-1/TGF-β and daf-12/NHR steroid hormone signaling pathways are required for the daf-16/FOXO arrest-defective phenotype, suggesting that daf-16/FOXO represses dbl-1/TGF-β and daf-36. The dbl-1/TGF-β and daf-12/NHR pathways have not previously been shown to affect L1 development, but we found that disruption of these pathways delayed L1 development in fed larvae, consistent with these pathways promoting development in starved daf-16/FOXO mutants. Though the dbl-1/TGF-β and daf-12/NHR pathways are epistatic to daf-16/FOXO for the arrest-defective phenotype, disruption of these pathways does not suppress starvation sensitivity of daf-16/FOXO mutants. This observation uncouples starvation survival from developmental arrest, indicating that DAF-16/FOXO targets distinct effectors for each phenotype, and revealing that inappropriate development during starvation does not cause the early demise of daf-16/FOXO mutants. Overall, this study shows that daf-16/FOXO promotes developmental arrest cell-nonautonomously by repressing pathways that promote larval development.
2016-05-27 | GSE69329 | GEO
Project description:Investigation of whole genome gene expression level changes in C. elegans genes daf-9 and daf-12 mutant,compared to the wild-type strain NimbleScan softwareM-bM-^@M-^Ys implementation of RMA offers quantile normalization and background correction. There are three steps of RMA: Firstly, background subtraction was performed using a local background estimator. Secondly, quantile normalization (Bioinformatics 2003; 19:185) at probe level was done to make the expression distributions the same for all arrays. Last, probe set summarization was performed using Robust Multichip Average (RMA) algorithm as described by Irizarry, et al. (Nucleic Acids Res. 2003; 31:e15 and Biostatistics 2003; 4:249). A nine chip study using total RNA recovered from three separate wild-type cultures of C.elegans and three separate cultures of daf-9 mutantM-oM-<M-^Lthree separate cultures of daf-12 mutant.The C. elegans 12 x 135K Gene Expression Array was manufactured by Roche NimbleGen. This array enables you to conveniently and simultaneously hybridize 12 samples on each slide. About 13,187 genes are collected from the authoritative data source including Wormbase.
2012-10-18 | E-GEOD-41661 | biostudies-arrayexpress
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:Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification
2007-02-08 | GSE5801 | GEO
Project description:Animals change developmental fates in response to external cues. In the nematode Caenorhabditis elegans, unfavorable environmental conditions induce a state of diapause known as dauer by inhibiting the conserved DAF-2 insulin-like signaling (ILS) pathway through incompletely understood mechanisms. We previously established a role for the C. elegans dosage compensation protein DPY-21 in the control of dauer arrest and DAF-2 ILS. Here we show that dosage compensation acts through the histone H4 lysine 20 methyltransferase SET-4 to promote dauer arrest in part by repressing the X-linked ins-9 gene, which encodes a new agonist insulin-like peptide (ILP) expressed specifically in the paired ASI sensory neurons that are required for dauer bypass. ins-9 repression in dauer-constitutive mutants requires DPY-21, SET-4, and the FoxO transcription factor DAF-16, which is the main target of DAF-2 ILS. In contrast, autosomal genes encoding major agonist ILPs that promote reproductive development are not repressed by DPY-21, SET-4, or DAF-16/FoxO. Our results implicate the dosage compensation machinery as a sensory rheostat that reinforces developmental fates in response to environmental cues by modulating autocrine and paracrine DAF-2 ILS.
2017-02-28 | GSE89295 | GEO