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Gene expression profile of E1A infected C2C12 myotubes

ABSTRACT: Proliferating C2C12 myoblasts were induced to differentiate into myotubes and then infected with adenovirus expressing E1A (Ad-E1A), which induces cell cycle re-entry and dedifferentiation. We analyzed the transcriptional profile of E1A infected C2C12-myotubes through the Affymetrix Mouse Genome 430 2.0 Array, searching for genes that were significantly regulated between two independent biological replicates at two different time points (24h and 36h after infection with Ad-E1A). In addition, we took advantage of the E1A mutant known as YH47/dl928 (hereafter referred as YH47), which bears two mutations in the pocket-binding region of E1A (Y48H, C124G) able to disrupt the interaction with Rb and its cognate proteins and to impair cell-cycle re-entry phenotype. YH47 mutant was used to identify the Rb independent transcriptional reprogramming of C2C12.

ORGANISM(S): Mus musculus

PROVIDER: GSE28457 | GEO | 2012/05/31

SECONDARY ACCESSION(S): PRJNA139223

REPOSITORIES: GEO

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Gene expression profile of E1A infected C2C12 myotubes

Project description:Proliferating C2C12 myoblasts were induced to differentiate into myotubes and then infected with adenovirus expressing E1A (Ad-E1A), which induces cell cycle re-entry and dedifferentiation. We analyzed the transcriptional profile of E1A infected C2C12-myotubes through the Affymetrix Mouse Genome 430 2.0 Array, searching for genes that were significantly regulated between two independent biological replicates at two different time points (24h and 36h after infection with Ad-E1A). In addition, we took advantage of the E1A mutant known as YH47/dl928 (hereafter referred as YH47), which bears two mutations in the pocket-binding region of E1A (Y48H, C124G) able to disrupt the interaction with Rb and its cognate proteins and to impair cell-cycle re-entry phenotype. YH47 mutant was used to identify the Rb independent transcriptional reprogramming of C2C12. C2C12 cells were differentiated in vitro to myotubes as previously described. Myotubes were, then, infected with an adenovirus carrying the 12S form of E1A (dl520), with the YH47 E1A mutant (dl928) or with a control adenovirus (CTR) expressing a deletion of essentially the entire E1A gene (dl312). Two different time points after infection were considered (24 hours and 36 hours) to evaluate changes in C2C12 cells expression profile. Technical (A or B) and biological replicates (EXP1 or EXP2) were done for each condition.

2012-05-30 | E-GEOD-28457 | biostudies-arrayexpress

Adenovirus E1A oncogene induces re-replication of cellular DNA and alters DNA replication dynamics

Project description:Human adenovirus type 5 oncogene E1A was shown to induce massive re-replication of cellular DNA in late S phase. Using DNA combing analysis, it was shown that DNA replication dynamics including replicon length, fork velocity and inter-origin distance were dramatically altered in E1A expressing cells as compared to that of normal serum stimulated cells. It was also shown that c-Myc that is induced in E1A expressing cells is essential for the efficient entry of E1A expressing cells into S phase. Serum starved cells were infected with an adenovirus expressing only the transforming E1A protein, and with Adbeta-galactosidase (control) were analyzed by flow cytomery. DNA prepared from such cells were analyzed by DNA combing analysis and data obtained were examined statistically. Requirement of Myc in E1A induced S phase entry was also examined by using antisense Myc vector.

2013-05-22 | E-GEOD-47140 | biostudies-arrayexpress

Adenovirus E1A oncogene induces re-replication of cellular DNA and alters DNA replication dynamics

2013-05-22 | GSE47140 | GEO

Expression profiles and ChIP on chip genomewide experiments with dl1500 virus (expressing WT small e1a).

Project description:Adenovirus e1a induces quiescent human cells to divide. We found that e1a causes global relocalization of the RB-proteins (RB, p130, p107) and p300/CBP histone acetyltransferases on promoters that restricts H3K18ac to a limited set of genes to stimulate cell cycling and inhibit antiviral responses and cellular differentiation. Soon after expression, e1a binds transiently to cell cycle/growth genes, causing enrichment of p300/CBP, PCAF, H3K18ac, depletion of RB-proteins, and transcriptional activation. e1a also associates transiently with antiviral genes, causing enrichment for RB, p130, H4K16ac, increased nucleosome density, and repression. At later times, e1a and p107 bind mainly to development/differentiation genes, repressing transcription. The temporal order of e1a binding required its interactions with p300/CBP and RB-proteins. Our data uncover a defined transcriptional and epigenetic reprogramming leading to cellular transformation.

2008-08-26 | GSE12045 | GEO

Profiles and ChIP on chip experiments with dl1500 virus (expressing WT small e1a), R2G and deltaCR2 mutant viruses

2008-08-26 | GSE12543 | GEO

Expression profiles and ChIP on chip genomewide experiments with dl1500 virus (expressing WT small e1a).

2008-08-26 | E-GEOD-12045 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [RB1_ChIP]

Project description:Oncogenic transformation by adenovirus small e1a depends on simultaneous interactions with P300/CBP and RB proteins. To understand why, experiments with structure-based e1a mutants were analyzed with RNA- and ChIP-seq. The results indicate that e1a displaces RBs from E2F activation domains and, by promoting P300 acetylation of RB1 K873/K874, locks them into a repressing conformation that interacts with repressive chromatin modifying enzymes. e1a then delivers these repressing p300-e1a-RB1 complexes to cell genes that have unusually high P300 association with the gene body, enriched in genes of the TGFb-, TNF-, and IL1-signaling pathways. The P300-e1a-RB complex condenses chromatin, dependent on HDAC activity, P300 lysine acetylase activity, the P300 bromodomain, and acetylation of RB K873/K874 and e1a K239, contributing to repression of host genes that would otherwise inhibit cell cycling. The data suggest why e1a must bind P300/CBP as well as RBs for oncogenic transformation and why a trimeric P300-e1a-RB1 complex is required. Examination of RB1 rearrangements by adenoviral e1a in IMR90

2014-08-15 | E-GEOD-59689 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [Pol2_ChIP]

2014-08-15 | E-GEOD-59691 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [RB1_ChIP_2]

2014-08-15 | E-GEOD-59690 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [IMR90_Input]

Project description:Oncogenic transformation by adenovirus small e1a depends on simultaneous interactions with P300/CBP and RB proteins. To understand why, experiments with structure-based e1a mutants were analyzed with RNA- and ChIP-seq. The results indicate that e1a displaces RBs from E2F activation domains and, by promoting P300 acetylation of RB1 K873/K874, locks them into a repressing conformation that interacts with repressive chromatin modifying enzymes. e1a then delivers these repressing p300-e1a-RB1 complexes to cell genes that have unusually high P300 association with the gene body, enriched in genes of the TGFb-, TNF-, and IL1-signaling pathways. The P300-e1a-RB complex condenses chromatin, dependent on HDAC activity, P300 lysine acetylase activity, the P300 bromodomain, and acetylation of RB K873/K874 and e1a K239, contributing to repression of host genes that would otherwise inhibit cell cycling. The data suggest why e1a must bind P300/CBP as well as RBs for oncogenic transformation and why a trimeric P300-e1a-RB1 complex is required. Chromatin IP background Input DNA for ChIP-seq normalization

2014-08-15 | E-GEOD-59692 | biostudies-arrayexpress

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