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A general mechanism for transcription regulation by Oct1 and Oct4 in response to genotoxic and oxidative stress

ABSTRACT: We identify inducible binding of the transcription factor Oct1 to numerous targets following exposure to hydrogen peroxide. Oct1 bound ChIP fragments were sequenced in the presence and absence of H2O2 exposure using HeLa cells. Both 26 and 36bp reads were generated. Each processed file contains a list of genomic regions (NCBI 36.1, H_sapiens_Mar_2006, hg18) enriched for Oct1 binding. These files were generated by running the EnrichedRegionMaker on ScanSeqs window scored data, see http://useq.sourceforge.net/ . Adjacent and overlapping windows with a q-value FDR of 0.0001 were joined into larger enriched regions. The best scoring window's scores are used to represent the enriched region.

ORGANISM(S): Homo sapiens

SUBMITTER: Dean Tantin

PROVIDER: E-GEOD-14283 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A general mechanism for transcription regulation by Oct1 and Oct4 in response to genotoxic and oxidative stress.

Kang Jinsuk J Gemberling Matthew M Nakamura Mitsuhiro M Whitby Frank G FG Handa Hiroshi H Fairbrother William G WG Tantin Dean D

Genes & development 20090101 2

Oct1 and Oct4 are homologous transcription factors with similar DNA-binding specificities. Here we show that Oct1 is dynamically phosphorylated in vivo following exposure of cells to oxidative and genotoxic stress. We further show that stress regulates the selectivity of both proteins for specific DNA sequences. Mutation of conserved phosphorylation target DNA-binding domain residues in Oct1, and Oct4 confirms their role in regulating binding selectivity. Using chromatin immunoprecipitation, we ...[more]

PMID: 19171782

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2015-09-17 | E-GEOD-65918 | biostudies-arrayexpress

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2016-04-01 | E-GEOD-77650 | biostudies-arrayexpress

Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [HiChIP]

Project description:The pathways used by cells to transition between pluripotent and tissue-specific states are incompletely understood. Here we show that the widely-expressed transcription factor Oct1/Pou2f1 activates silent, developmental lineage-appropriate genes to “canalize” developmental progression. Using Oct1 inducible knockout embryonic stem cells, we show that that Oct1 deficiency impairs mesodermal and terminal muscle differentiation in a manner that can be rescued by Oct1 retroviral expression. We show that mesoderm-specific genes are not correctly induced early in the differentiation timecourse. Oct1-deficient cells lose temporal coherence in the induction of lineage-specific genes and show inappropriate developmental lineage branching, resulting in poorly differentiated cells states retaining epithelial characteristics. In embryonic stem cells, Oct1 co-binds with Oct4 to genes critical for mesoderm induction, and continues to bind these genes during differentiation. Oct1 binding events are enriched at the termini of chromatin loops, including loops gained with differentiation. The Utx/Kdm6a histone lysine demethylase also binds to many of these genes, and using a prototypic Pax3 gene we show that Oct1 recruits Utx to remove inhibitory H3K27me3 marks and activate expression. The specificity of the ubiquitous Oct1 protein for mesodermal genes can be explained by cooperative interactions with lineage-driving Smad transcription factors, as we show that Smad and Oct binding sites frequently coexist mesoderm-specific genes, and that Oct1 and Smad3 act cooperatively at the Myog enhancer. Overall, these results identify Oct1 as a key mediator of the induction of mesoderm lineage-specific genes.

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Effects of Oct1 inhibition in AR signaling

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2017-11-30 | GSE98831 | GEO

Combinatorial binding of transcription factors in the pluripotency control regions of the genome

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Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [BulkRNAseq7221]

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