Dataset Information


Reduced representation bisulfite sequencing from G0 & G4/G5 CMP

ABSTRACT: Differential hyper- and hypo-methylation regions in G0 versus G4/G5 CMP The goal of this study is to evaluate changes in CpG methylation profilings of telomere dysfunctional common myeloid progenitor cells (CMP) as compared to their wild type controls Genomic DNA was extracted from sorted CMP populations isolated from 3 pools of G0 or 2 pools of G5 mice using UltraPure Phenol:Chloroform:Isoamyl Alcohol according to manufacturer’s instructions (Life Technologies). 14,000 to 30,000 cells were available for each sample, resulting in a minimum of 45ng of DNA. Genome-wide DNA methylation profiling was performed by RRBS. Library preparation and sequencing were performed at the UT MD Anderson Cancer Center’s DNA Methylation Analysis Core and Sequencing and Microarray Facility, according to published protocols. RRBS sequencing data were aligned and methylation was called using Bismark v0.7.119. In brief, bisulphite-treated DNA was aligned to UCSC Genome Browser mm10 reference genome using Bowtie. In total 29-38 million reads were generated per sample with alignment rates around 63%. Next, MethylKit10 implemented with Fisher’s exact test was used to compare the cytosine methylation profiles of G0 and G5 CMP. Gene promoter regions were calculated based on RefSeq gene annotations with regions starting 1 kb upstream of the annotated transcription start site (TSS) and extending 500 base pairs downstream of TSS. Exons, introns, and CpG islands coordinates were collected from the UCSC Genome Browser mm10 version.

ORGANISM(S): Mus musculus  

SUBMITTER: Derrick Ong   Ronald Depinho  Simona Colla  Ting Gong 

PROVIDER: E-GEOD-62392 | ArrayExpress | 2015-04-09



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Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome.

Colla Simona S   Ong Derrick Sek Tong DS   Ogoti Yamini Y   Marchesini Matteo M   Mistry Nipun A NA   Clise-Dwyer Karen K   Ang Sonny A SA   Storti Paola P   Viale Andrea A   Giuliani Nicola N   Ruisaard Kathryn K   Ganan Gomez Irene I   Bristow Christopher A CA   Estecio Marcos M   Weksberg David C DC   Ho Yan Wing YW   Hu Baoli B   Genovese Giannicola G   Pettazzoni Piergiorgio P   Multani Asha S AS   Jiang Shan S   Hua Sujun S   Ryan Michael C MC   Carugo Alessandro A   Nezi Luigi L   Wei Yue Y   Yang Hui H   D'Anca Marianna M   Zhang Li L   Gaddis Sarah S   Gong Ting T   Horner James W JW   Heffernan Timothy P TP   Jones Philip P   Cooper Laurence J N LJ   Liang Han H   Kantarjian Hagop H   Wang Y Alan YA   Chin Lynda L   Bueso-Ramos Carlos C   Garcia-Manero Guillermo G   DePinho Ronald A RA  

Cancer cell 20150501 5

Myelodysplastic syndrome (MDS) risk correlates with advancing age, therapy-induced DNA damage, and/or shorter telomeres, but whether telomere erosion directly induces MDS is unknown. Here, we provide the genetic evidence that telomere dysfunction-induced DNA damage drives classical MDS phenotypes and alters common myeloid progenitor (CMP) differentiation by repressing the expression of mRNA splicing/processing genes, including SRSF2. RNA-seq analyses of telomere dysfunctional CMP identified aber  ...[more]

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