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Proteomics of liver from mice fed high fat diet (HFD) or regular chow diet

ABSTRACT: Proteomics of liver tissue from mice fed a high fat diet (HFD) or regular chow diet. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Moshe Shay Ben-Haim

LAB HEAD: Gideon Rechavi

PROVIDER: PXD029280 | Pride | 2021-10-27

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	QEP2_GRE_CHOW15_1_F1a_170316.dat	Other
	QEP2_GRE_CHOW15_1_F1a_170316.raw	Raw
	QEP2_GRE_CHOW15_1_F2a_140316.dat	Other
	QEP2_GRE_CHOW15_1_F2a_140316.raw	Raw
	QEP2_GRE_CHOW15_1_F3a_170316.dat	Other

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Publications

Dynamic regulation of N6,2'-O-dimethyladenosine (m6Am) in obesity.

Ben-Haim Moshe Shay MS Pinto Yishay Y Moshitch-Moshkovitz Sharon S Hershkovitz Vera V Kol Nitzan N Diamant-Levi Tammy T Beeri Michal Schnaider MS Amariglio Ninette N Cohen Haim Y HY Rechavi Gideon G

Nature communications 20211210 1

The prevalent m6Am mRNA cap modification was recently identified as a valid target for removal by the human obesity gene FTO along with the previously established m6A mRNA modification. However, the deposition and dynamics of m6Am in regulating obesity are unknown. Here, we investigate the liver m6A/m methylomes in mice fed on a high fat Western-diet and in ob/ob mice. We find that FTO levels are elevated in fat mice, and that genes which lost m6< ...[more]

PMID: 34893620

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Proteomics of HEPG2 cells following FTO overexpression and knockdown

Project description:Proteomics of HEPG2 cells following FTO overexpression and knockdown. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021

2021-10-27 | PXD029268 | Pride

Proteomics of liver from ob/ob and WT mice

Project description:Proteomics of liver tissue from ob/ob and WT mice. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021

2021-10-27 | PXD029217 | Pride

m6Am sequesters PCF11 to promote full-length transcription [catabolicSLAM]

Project description:RNA modifications regulate how RNAs metabolize and function to impact development and diseases. N6,2’-O-dimethyladenosine (m6Am) is one such modification and despite being abundant, m6Am function remains unclear. Here, we identified cleavage and polyadenylation factor, PCF11 as a m6Am-specific binding protein. Direct quantification of mature versus nascent RNAs revealed that m6Am does not regulate mRNA stability but promotes transcription of nascent RNAs. m6Am caused RNA Polymerase II (Pol II) to be more processive when transcribing m6Am-modified RNAs. Rather than PCF11 regulating m6Am-modified RNA, m6Am sequesters PCF11 away from proximal Pol II, suppressing premature dissociation of elongating Pol II and promoting Pol II full-length transcription of m6Am-modified RNAs. This establishes a mechanism through which an RNA modification regulates transcription.

2024-10-31 | GSE234135 | GEO

m6Am sequesters PCF11 to promote full-length transcription [ChIP-Seq]

2024-10-31 | GSE233877 | GEO

m6Am sequesters PCF11 to promote full-length transcription [anabolicSLAM]

2024-10-31 | GSE234133 | GEO

m6Am sequesters PCF11 to promote full-length transcription [PCT]

2024-10-31 | GSE234131 | GEO

m6Am sequesters PCF11 to promote full-length transcription [m6ACE]

2024-10-31 | GSE254149 | GEO

m6Am sequesters PCF11 to promote full-length transcription [RNA-seq]

2024-10-31 | GSE254148 | GEO

m6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we investigated the effect of gene deletion of Mettl3, a m6A methyltransferase, and Fto, a m6A and m6Am demethlyase, induced in adulthood in excitatory neurons of the neocortex and hippocampus (Camk2a-Cre Mettl3 or Fto cKO) on the cortical epitranscriptome. PolyA-RNA-fragments from 3-5 replicates per group were processed both as m6A/m-sample (RNA immunoprecipiation RIP with an m6A and m6Am antibody) and RNA-input sample.

2018-07-10 | GSE113793 | GEO

m6Am sequesters PCF11 to suppress premature termination and drive neuroblastoma differentiation [fPAR-CLIP]

Project description:N6,2’-O-dimethyladenosine (m6Am) is an abundant mRNA modification that impacts multiple diseases but its function remains controversial since the m6Am reader is unknown. Using quantitative proteomics, we identified transcriptional terminator PCF11 as a m6Am-specific reader. Direct quantification of mature versus nascent RNAs reveals m6Am does not regulate mRNA stability but promotes nascent transcription. Mechanistically, m6Am functions by sequestering PCF11 away from proximal RNA Pol II. This suppresses PCF11 from dissociating Pol II near transcription start sites, thereby promoting full-length transcription of m6Am-modified RNAs. m6Am’s unique relationship with PCF11 means m6Am function is enhanced when PCF11 is reduced, which occurs during all-trans-retinoic-acid (ATRA) induced neuroblastoma-differentiation therapy. Here, m6Am promotes expression of ATF3, a repressor of the neuroblastoma biomarker MYCN. Depleting m6Am suppresses MYCN-repression in ATRA-treated neuroblastoma and maintains their tumour stem-like properties. Collectively, we characterize m6Am as an anti-terminator RNA modification that suppresses premature termination and modulates neuroblastoma therapeutic response.

2024-10-31 | GSE266116 | GEO