Title | Genomic and proteomic analysis of transcription factor TFII-I reveals insight into the response to cellular stress. |
Publication Type | Journal Article |
Year of Publication | 2014 |
Authors | Fan, AXiucheng, Papadopoulos, GL, Hossain, MA, Lin, I-J, Hu, J, Tang, TMing, Kilberg, MS, Renne, R, Strouboulis, J, Bungert, J |
Journal | Nucleic Acids Res |
Volume | 42 |
Issue | 12 |
Pagination | 7625-41 |
Date Published | 2014 Jul |
ISSN | 1362-4962 |
Keywords | Activating Transcription Factor 3, Binding Sites, Biotinylation, Carbon-Nitrogen Ligases, DNA Topoisomerases, Type II, Elongin, Escherichia coli Proteins, Genomics, Humans, K562 Cells, Nuclear Proteins, Proteomics, Repressor Proteins, RNA Polymerase II, Stress, Physiological, TATA-Binding Protein Associated Factors, Transcription Factors, Transcription Factors, TFII, Transcription Initiation Site |
Abstract | The ubiquitously expressed transcription factor TFII-I exerts both positive and negative effects on transcription. Using biotinylation tagging technology and high-throughput sequencing, we determined sites of chromatin interactions for TFII-I in the human erythroleukemia cell line K562. This analysis revealed that TFII-I binds upstream of the transcription start site of expressed genes, both upstream and downstream of the transcription start site of repressed genes, and downstream of RNA polymerase II peaks at the ATF3 and other stress responsive genes. At the ATF3 gene, TFII-I binds immediately downstream of a Pol II peak located 5 kb upstream of exon 1. Induction of ATF3 expression increases transcription throughout the ATF3 gene locus which requires TFII-I and correlates with increased association of Pol II and Elongin A. Pull-down assays demonstrated that TFII-I interacts with Elongin A. Partial depletion of TFII-I expression caused a reduction in the association of Elongin A with and transcription of the DNMT1 and EFR3A genes without a decrease in Pol II recruitment. The data reveal different interaction patterns of TFII-I at active, repressed, or inducible genes, identify novel TFII-I interacting proteins, implicate TFII-I in the regulation of transcription elongation and provide insight into the role of TFII-I during the response to cellular stress. |
DOI | 10.1093/nar/gku467 |
Alternate Journal | Nucleic Acids Res |
PubMed ID | 24875474 |
PubMed Central ID | PMC4081084 |
Grant List | R01 CA088763 / CA / NCI NIH HHS / United States R01DK09062 / DK / NIDDK NIH HHS / United States R01DK094729 / DK / NIDDK NIH HHS / United States R01DK083389 / DK / NIDDK NIH HHS / United States |
Genomic and proteomic analysis of transcription factor TFII-I reveals insight into the response to cellular stress.
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