# _embedded.samples[].characteristics.submission description[].text
In order to gain insight into the effects of aging on susceptibility to environmental toxins, we characterized the expression of xenobiotic metabolizing enzymes (XMEs) from the livers of male Brown Norway and F344 rats across the adult lifespan. To examine metabolic processes across lifespan after challenge with a xenobiotic compound, Brown Norway rats were exposed to 1.0 g/kg body weight toluene by oral gavage in corn oil (4ml/kg body weight) or corn oil alone. Experiment Overall Design: Brown Norway rats: Analysis of gene expression profiles for XMEs in male Brown Norway rats 4, 12, and 24 months old. Rats were exposed to 1g/kg toluene by oral gavage, and sacrificed after 4 hours. Total RNA was isolated from liver samples and gene expression analyzed using Affymetrix Rat 230 2.0 full-genome GeneChips. Data from 18 samples, with three rats in each of the control age groups and dosed age groups, were analyzed. Experiment Overall Design: F344 rats: Analysis of gene expression profiles for XMEs in male F344 6, 11, 18, and 24 months old. Total RNA was isolated from liver samples and gene expression analyzed using Affymetrix Rat 230 2.0 full-genome GeneChips. Data from 16 samples, with four rats in each of the 4 age groups, were analyzed.

# _embedded.samples[].characteristics.submission title[].text
Transcription profiling of male rats Brown Norway and F344 reveals coordinated changes in xenobiotic metabolizing enzyme gene expression in aging

# _embedded.samples[].characteristics.submission description[].text
Dosage compensation in mammals occurs at two levels. In addition to balancing X-chromosome dosage between males and females via X-inactivation, mammals also balance dosage of Xs and autosomes. It has been proposed that X-autosome equalization occurs by upregulation of Xa (active X). To investigate the mechanism, we perform allele-specific ChIP-seq for chromatin epitopes and analyze RNA-seq data (SRA010053). The hypertranscribed Xa demonstrates enrichment of active chromatin marks relative to autosomes. We derive predictive models for relationships among Pol II, active mark densities and gene expression, and we suggest that Xa upregulation involves increased transcription initiation and elongation. Enrichment of active marks on Xa does not scale proportionally with transcription output, a disparity explained by nonlinear quantitative dependencies among active histone marks, Pol II occupancy and transcription. Notably, the trend of nonlinear upregulation also occurs on autosomes. Thus, Xa upregulation involves combined increases of active histone marks and Pol II occupancy, without invoking X-specific dependencies between chromatin states and transcription. Examination of 4 marks of active transcription (H3K4me3, H3K36me3, POL-II-S2P, POL-II-S5P) in a transformed female mouse embryonic fibroblast cell line (EY.T4).

# _embedded.samples[].characteristics.submission title[].text
X-chromosome hyperactivation in mammals via nonlinear relationships between chromatin states and transcription

# _embedded.samples[].organization[].Name
Howard Hughes Medical Inst, Mass General Hospital, Harvard Medical School

# _embedded.samples[].organization[].Name
Howard Hughes Medical Inst, Mass General Hospital, Harvard Medical School

# _embedded.samples[].characteristics.secondary description[].text
HUVECs transduced with control oligonucleotide and GFP, sorted for fluorescence positive population

# _embedded.samples[].characteristics.tranducer[].text
control oligonucleotide and GFP, sorted for fluorescence positive population

# _embedded.samples[].organization[].Name
Institute for Cancer Research and Treatment, University of Torino

# _embedded.samples[].characteristics.secondary description[].text
HUVECs transduced with mir-126 antisense oligonucleotide and GFP, sorted for fluorescence positive population

# _embedded.samples[].characteristics.tranducer[].text
mir-126 antisense oligonucleotide and GFP, sorted for fluorescence positive population

# _embedded.samples[].organization[].Name
Institute for Cancer Research and Treatment, University of Torino

# _embedded.samples[].characteristics.secondary description[].text
HUVECs transduced with GFP, sorted for fluorescence positive population

# _embedded.samples[].characteristics.tranducer[].text
GFP, sorted for fluorescence positive population

# _embedded.samples[].organization[].Name
Institute for Cancer Research and Treatment, University of Torino

# _embedded.samples[].characteristics.sample source name[].text
Transformed mouse embryonic fibroblast line, H3K36me3 ChIP

# _embedded.samples[].organization[].Name
Howard Hughes Medical Inst, Mass General Hospital, Harvard Medical School

# _embedded.samples[].organization[].Name
Washington University School of Medicine