Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

13 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene Expression Profile for knocking down Tet1 in pre-iPSCs culturing in Vc medium.

ABSTRACT: Tet1 is a hydroxylase known for its role in the conversion of 5-methylcytosines (5mC) to 5-hydroxymethylcytosines (5hmC) involved in the possible active demethylation process and gene expression regulation. As somatic cell reprogramming involves the re-activation of pluripotency genes and the silencing of somatic ones, it remains unclear the role of Tet1 in the reprogramming process. Here, we performed RNAseq for WT and knocking down Tet1 in two pre-iPSCs cell lines, pre2-2 and pre3. Using two pre-iPSCs cell lines: pre2-2 and pre3, cultured by mES medium(+lif), transfected siCtrl/siTet1 siRNA or non-treatment, then, after 16h, the medium were replaced by mES(+lif) medium plus Vc(50ug/ml), total RNA was extracted after another 32h later for RNAseq.

ORGANISM(S): Mus musculus

SUBMITTER: Xiaoshan Wang

PROVIDER: E-GEOD-48206 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Vitamin C modulates TET1 function during somatic cell reprogramming.

Chen Jiekai J Guo Lin L Zhang Lei L Wu Haoyu H Yang Jiaqi J Liu He H Wang Xiaoshan X Hu Xiao X Gu Tianpeng T Zhou Zhiwei Z Liu Jing J Liu Jiadong J Wu Hongling H Mao Shi-Qing SQ Mo Kunlun K Li Yingying Y Lai Keyu K Qi Jing J Yao Hongjie H Pan Guangjin G Xu Guo-Liang GL Pei Duanqing D

Nature genetics 20131027 12

Vitamin C, a micronutrient known for its anti-scurvy activity in humans, promotes the generation of induced pluripotent stem cells (iPSCs) through the activity of histone demethylating dioxygenases. TET hydroxylases are also dioxygenases implicated in active DNA demethylation. Here we report that TET1 either positively or negatively regulates somatic cell reprogramming depending on the absence or presence of vitamin C. TET1 deficiency enhances reprogramming, and its overexpression impairs reprog ...[more]

PMID: 24162740

Similar Datasets

Tet1 as a Negative Regulator of Somatic Cell Reprogramming

Project description:Tet1 is a hydroxylase known for its role in the conversion of 5-methylcytosines (5mC) to 5-hydroxymethylcytosines (5hmC) involved in the possible active demethylation process and gene expression regulation1-5.M-BM- As somatic cell reprogramming involves the re-activation of pluripotency genes and the silencing of somatic ones6, it remains unclear whether Tet1 plays a positive or negative role in the reprogramming process. Here we show that Tet1 deficiency enhances reprogramming and its overexpression impairs reprogramming. Mechanistically, we demonstrated that Tet1 represses the early obligatory process of mesenchymal to epithelial transition (MET) during reprogramming7,8. Thus, our findings not only define a negative role for Tet1 in somatic cell reprogramming, but also suggest that the Tet enzymes regulate cell fate through distinctive mechanisms. Examination of genome DNA hmC modifications in 2 conditions: individually overexpressed Tet1CD or Tet2CD during MEF reprogramming; Examination of mRNA levels in five different conditions: individually overexpressed DR or Tet1CD or Tet1CDmut or Tet2CD or Tet2CDmut, during MEF reprogrammig.

2013-03-08 | E-GEOD-44935 | biostudies-arrayexpress

c-Jun impedes somatic cell reprogramming by activating mesenchymal core regulators and suppressing pluripotent ones

Project description:The somatic cell fate can be converted to tumor or pluripotent ones by ectopic expression of transcription factors in vitro and in vivo. Many oncogenic transcription factors are known to mediate both fates as they share similar proliferative and metabolic properties. Paradoxically, we found c-Jun as the first oncogene that appears to specify a somatic fate, oppose the pluripotent one and impede reprogramming. We performed a series of high through out sequencing to understand the way cJun works. To understand how c-Jun drives mESCs differentiating, we obtained c-Jun TetOn mESCs, and performed RNAseq 36h later with dox inducing or not . To understand why c-Jun blocks reprogramming while c-JunDN and Jdp2 can replace Oct4, we overexpressed these factors with KSM during reprogramming and performed RNAseq 3 Days after virus transfection. Moreover, to extend understand how these factors regulate gene expression, we also overexpressed these factors in MEF and performed RNAseq. Further more, to understand how cJun regulates cell fates and gene expression, we overexpressed c-Jun in mouse ESC and performed ChIP-seq. Also, we performed c-JunDN ChIP-seq during somatic cells reprogramming on day 3, to explore the binding sites of c-JunDN.

2015-06-10 | E-GEOD-50776 | biostudies-arrayexpress

Gene Expression Profile for knocking down Tet1 in pre-iPSCs culturing in Vc medium.

2013-10-27 | GSE48206 | GEO

Function of 5C medium in somatic cell reprogramming

Project description:We induced reprogramming by mES and 5C medium, and collected mRNA profiles of the GFP+ and GFP- reprogramming cells sorted by FACS. We found that 5C iPSCs showed differences with mES iPSCs, with different influences on GFP+ and GFP- cells on MET. And we picked the 5C iPSCs single colony, cultured with naive and primed medium. We showed that 5C iPSCs could be converted to naive and primed state respectively.

2019-04-14 | GSE103765 | GEO

5-hydroxymethylcytosine-mediated epigenetic modifications between iPSCs and hESCs

Project description:Mammalian somatic cells can be directly reprogrammed into induced pluripotent stem cells (iPSCs) by introducing defined sets of transcription factors. Somatic cell reprogramming involves epigenomic reconfiguration, conferring iPSCs with characteristics similar to embryonic stem (ES) cells. Human ES cells contain 5-hydroxymethylcytosine (5hmC), which is generated though the oxidation of 5-methylcytosine (5mC) by the TET family of enzymes. Here we show that 5hmC level increases significantly during reprogramming due to the activation of TET1. During this process, dynamic genome-wide 5hmC modification occurs across the genome with more modifications at telomere-proximal regions. Compared with hES cells, we found iPS cells tend to form large-scale (100kb-1.3Mb) aberrant reprogramming hotspots in subtelomeric regions, most of which display incomplete hydroxymethylation. Strikingly, these 5hmC aberrant hotspots largely coincide (>80%) with previously reported aberrant non-CG methylation regions. Our results suggest that 5hmC modification could play important roles during reprogramming to pluripotency, and contribute to the differences between iPSCs and hESCs. we generated comprehensive genome-wide profiles of 5hmC in somatic cells, iPS cell lines derived from a variety of origins, and multiple hES cell lines.

2013-03-21 | E-GEOD-37050 | biostudies-arrayexpress

Coordination of engineered factors with TET1/2 promotes early stage epigenetic modification during somatic cell reprogramming

Project description:Somatic cell reprogramming towards induced pluripotent stem cells (iPSCs) holds great promise in future regenerative medicine, however, the reprogramming process mediated by the traditional defined factors (OSNK) is slow and extremely inefficient. Here we show that a combination of modified reprogramming factors (OySyNyK), in which the transactivation domain of the Yes-associated protein is fused to OCT4, SOX2 and NANOG respectively, could be used to establish a highly efficient and rapid reprogramming system for iPSC generation. We show that the efficiency of OySyNyK-induced iPSCs was up to 100-fold higher than that of induction by traditional OSNK. Moreover we show that the reprogramming by OySyNyK is very rapid (initiated at 24 h versus 5 d by OSNK). Compared with OSNK, we found that OySyNyK factors significantly increased the expression of Tet1/2 at the early stage, which will interact with OSNK factors, and co-occupy pluripotency loci in the genome for somatic cell reprogramming. Our studies not only establish a rapid and highly efficient iPSC reprogramming system, but also uncover a novel mechanism by which OSNK factors coordinate with TET proteins to regulate 5hmC-mediated epigenetic control, thereby promoting somatic cell reprogramming. We examined DNA hydroxymethylation progression of reprogramming intermediates. To this end, we profiled the genome-wide 5hmC distribution in MEFs, the reprogramming intermediates at different stages induced by either the OSNK or OySyNyK methods, and iPSCs using the chemical capture approach

2013-08-08 | E-GEOD-46202 | biostudies-arrayexpress

The Role of Tet1 During Somatic Cell Reprogramming

2013-03-08 | GSE44935 | GEO

Chromatin-associated factors Dppa2 and Dppa4 guide epigenetic remodeling during reprogramming to pluripotency (RNA-seq)

Project description:As somatic cells are converted to iPSCs, their chromatin undergoes wide-ranging rearrangements that affect the ratio of euchromatin-to-heterochromatin, DNA methylation patterns and the regulation of enhancers and promoters. The molecular machinery underlying this process remains largely unknown. Here, we show that Dppa2 and Dppa4, two thus far poorly characterized mES-specific factors, play a key role in resetting the epigenome to a pluripotent configuration. They function as a heterodimer, are induced in late reprogramming intermediates, and are required for reprogramming. When overexpressed with OSKM factors, Dppa2/4 yield reprogramming efficiencies exceeding 75% of the starting culture and accelerate reprogramming kinetics, generating iPSCs in as little as 4 days. When chromatinbound, Dppa2/4 initiate global chromatin decompaction via the DNA damage response pathway, which subsequently activates mES promoters and enhancers and enables an efficient progression to pluripotency. Our work provides critical insights into how the epigenome is remodeled during cell fate transitions.

2018-08-30 | GSE117172 | GEO

Chromatin-associated factors Dppa2 and Dppa4 guide epigenetic remodeling during reprogramming to pluripotency (ChIP-seq)

2018-08-30 | GSE117171 | GEO

5-hydroxymethylcytosine-mediated epigenetic modifications between iPSCs and hESCs

2013-03-21 | GSE37050 | GEO