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Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation

ABSTRACT: Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation

OTHER RELATED OMICS DATASETS IN: E-GEOD-51786

PROVIDER: PRJNA227370 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1028850.fastq.gz	Fastqsanger.gz
	SRR1028851.fastq.gz	Fastqsanger.gz
	SRR1028852.fastq.gz	Fastqsanger.gz
	SRR1028843.fastq.gz	Fastqsanger.gz
	SRR1028853.fastq.gz	Fastqsanger.gz

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Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation

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2014-02-13 | E-GEOD-52304 | biostudies-arrayexpress

Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [RRBS]

Project description:We report a reprogrammable mouse system in which reprogramming factor expression in vivo can be controlled temporally by treatment with doxycycline (Dox). Transient expression of reprogramming factors in vivo results in tumor development in various tissues, consisting of undifferentiated dysplastic cells. We analyzed the kidney tumors developed in reprogrammable mice for global gene expressions and DNA methylations. Reprogrammable mice at 4 weeks of age were treated with Dox for 7 days followed by the withdrawal. Seven days after the withdrawal, kidney tumors were analyzed for gene expressions and DNA methylations with microarray and RRBS method, respectively. Normal kidney tissue at the same age and ES cells were analyzed as controls. To examine the early changes of gene expressions, transgene-expressing kidney cells were FACS sorted and they are utilized for microarray analysis. Primary liver tumors in reprogrammable mice and transplanted secondary kidney tumors in the subcutaneous tissues of immnodeficient mice were also analyzed for gene expressions.

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Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]

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Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-02-13 | GSE52304 | GEO

Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [RRBS]

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A conserved factor Dhp1/Rat1/Xrn2 triggers premature transcription termination and nucleates heterochromatin to promote gene silencing [sRNA-seq]

Project description:Co-transcriptional RNA processing and surveillance factors mediate heterochromatin formation in fission yeast. In addition to RNAi, RNA elimination machinery including MTREC (Mtl1-Red1 core) and the exosome are involved in facultative heterochromatin assembly, however, the exact mechanisms remain unclear. Here we show that RNA elimination factors cooperate with the conserved exoribonuclease Dhp1/Rat1/Xrn2, which couples pre-mRNA 3â-end processing to transcription termination, to promote premature termination and facultative heterochromatin formation at meiotic genes. Dhp1 also affects termination of transcripts at genes that are targets of RNAi-mediated heterochromatin assembly. Moreover, Dhp1 facilitates constitutive heterochromatin formation and silencing at centromeric and mating-type loci. Remarkably, we find that Dhp1 interacts with the Clr4/Suv39h methyltransferase complex and acts directly to nucleate heterochromatin. Our results uncover a novel role for 3â-end processing and termination machinery in gene silencing through premature termination and suggest that non-canonical termination by Dhp1 and RNA elimination factors is linked to heterochromatin assembly. These findings have important implications for understanding mechanisms of gene silencing in higher eukaryotes. Sequencing and analysis of small RNA in two S. pombe mutants

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mRNA decapping factors and the exonuclease Xrn2 function in widespread premature termination of RNA polymerase II transcription

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Selective roles of vertebrate PCF11 in premature and full-length transcript termination (ChIP-seq)

Project description:The pervasive nature of RNA polymerase II (Pol II) transcription requires efficient termination. A key player in this process is the cleavage and polyadenylation (CPA) factor PCF11, which directly binds to the Pol II C-terminal domain and dismantles elongating Pol II from DNA in vitro. We demonstrate that PCF11-mediated termination is essential for vertebrate development. A range of genomic analyses, including: mNET-seq, 3’ mRNA-seq, chromatin RNA-seq and ChIP-seq, reveals that PCF11 enhances transcription termination and stimulates early polyadenylation genome-wide. PCF11 binds preferentially between closely spaced genes, where it prevents transcriptional interference and downstream gene silencing. Notably, PCF11 is sub-stoichiometric to the CPA complex. Low levels of PCF11 are maintained by an auto-regulatory mechanism involving premature termination of its own transcript, and are important for normal development. Both in human cell culture and during zebrafish development, PCF11 selectively attenuates the expression of other transcriptional regulators by premature CPA and termination.

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