Gene network transitions in embryos depend upon interactions between a pioneer transcription factor and core histones
| Autor: | Isabel Cuesta, Makiko Iwafuchi, Pilar Santisteban, Kenneth S. Zaret, Naomi Takenaka, Greg Donahue, Heinrich Roder, Steven H. Seeholzer, Anna B. Osipovich, Mark A. Magnuson |
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| Přispěvatelé: | Japan Society for the Promotion of Science, Astellas Pharma, Uehara Memorial Foundation for International Students, Comunidad de Madrid, Ministerio de Economía y Competitividad (España), European Commission, National Institutes of Health (US) |
| Rok vydání: | 2020 |
| Předmět: |
Transcription
Genetic Gene regulatory network Biology Article Cell Line Histones Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Transcription (biology) Genetics Animals Humans Nucleosome Gene Regulatory Networks Amino Acid Sequence Transcription factor 030304 developmental biology Regulation of gene expression 0303 health sciences Gene Expression Regulation Developmental DNA Chromatin Nucleosomes Cell biology Mice Inbred C57BL Histone chemistry biology.protein Female 030217 neurology & neurosurgery Transcription Factors |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname Nature genetics |
| Popis: | Gene network transitions in embryos and other fate-changing contexts involve combinations of transcription factors. A subset of fate-changing transcription factors act as pioneers; they scan and target nucleosomal DNA and initiate cooperative events that can open the local chromatin. However, a gap has remained in understanding how molecular interactions with the nucleosome contribute to the chromatin-opening phenomenon. Here we identified a short α-helical region, conserved among FOXA pioneer factors, that interacts with core histones and contributes to chromatin opening in vitro. The same domain is involved in chromatin opening in early mouse embryos for normal development. Thus, local opening of chromatin by interactions between pioneer factors and core histones promotes genetic programming. M.I. was supported by postdoctoral fellowships from Japan Society for the Promotion of Science Foundation (H26-683), Naito Foundation (RYU10000032), Astellas Foundation for Research on Metabolic Disorders (K0076) and Uehara Memorial Foundation (H24-20124). P.S. was supported by grant nos. SAF2016-75531-R (MICINN/FEDER, UE) and B2017/BMD-3724 (Comunidad de Madrid). The research was supported by NIH grant no. GM36477 to K.S.Z. |
| Databáze: | OpenAIRE |
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