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C. elegans wild type compared to vhl-1(ok161) RBPome and Proteome

ABSTRACT: We performed RNA interactome capture in wild type compared to vhl-1(ok161) loss-of-function worms. These data are combined with the proteome to distinguish changes in RBP abundance from differential binding events.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Caenorhabditis Elegans

SUBMITTER: Francesca Fabretti

LAB HEAD: Bernhard Schermer

PROVIDER: PXD014469 | Pride | 2020-01-08

REPOSITORIES: Pride

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			Action	DRS
	20180711_Q2_CF_ColID_604_ProjID_1283_Benzing_1_150.raw	Raw
	20180711_Q2_CF_ColID_604_ProjID_1283_Benzing_1_90.raw	Raw
	20180711_Q2_CF_ColID_604_ProjID_1283_Benzing_2_150.raw	Raw
	20180711_Q2_CF_ColID_604_ProjID_1283_Benzing_2_90.raw	Raw
	20180711_Q2_CF_ColID_604_ProjID_1283_Benzing_3_150.raw	Raw

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1 - 5 of 32

Publications

Activation of Hypoxia-Inducible Factor Signaling Modulates the RNA Protein Interactome in Caenorhabditis elegans.

Esmaillie Reza R Ignarski Michael M Bohl Katrin K Krüger Tim T Ahmad Daniyal D Seufert Lisa L Schermer Bernhard B Benzing Thomas T Müller Roman-Ulrich RU Fabretti Francesca F

iScience 20191127

The cellular response to hypoxia is crucial to organismal survival, and hypoxia-inducible factors (HIF) are the key mediators of this response. HIF-signaling is central to many human diseases and mediates longevity in the nematode. Despite the rapidly increasing knowledge on RNA-binding proteins (RBPs), little is known about their contribution to hypoxia-induced cellular adaptation. We used RNA interactome capture (RIC) in wild-type Caenorhabditis elegans and vhl-1 loss-of-function mutants to fi ...[more]

PMID: 31835171

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RNA-binding proteins associating with the 3’UTR of the ATP6V1A transcript in SIRT1 knock-down cells

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Secretome analysis of polarised macrophages derived from induced pluripotent stem cells

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IP of 5-methylcytosine (5-mc) enriched DNA fragments from control and mice with non-acoholic steatohepatitis (NASH) related hepatocellular carcinoma (HCC)

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-mc is a well establisehd epigenetic mark typically related to gene silencing events. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in liver tumours of high fat diet exposed mice who have progressed through NASH. Samples: 5mC profiles in livers of 2 control and 2 NASH driven HCC samples

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