Gene network transitions in embryos depend upon interactions between a pioneer transcription factor and core histones
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...
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| Published in | Nature genetics Vol. 52; no. 4; pp. 418 - 427 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.04.2020
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1061-4036 1546-1718 1546-1718 |
| DOI | 10.1038/s41588-020-0591-8 |
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| Abstract | 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.
An α-helical region conserved among FOXA pioneer factors interacts with core histones and promotes chromatin opening in vitro. This region also promotes chromatin opening in early mouse embryos and is required for normal development. |
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| AbstractList | 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. But a gap has remained in understanding how molecular interactions with the nucleosome contribute to the chromatin-opening phenomenon. Here we identified a short alpha-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. 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 [alpha]-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. 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.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. 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 [alpha]-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. An [alpha]-helical region conserved among FOXA pioneer factors interacts with core histones and promotes chromatin opening in vitro. This region also promotes chromatin opening in early mouse embryos and is required for normal development. 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. 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 a-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. 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. An α-helical region conserved among FOXA pioneer factors interacts with core histones and promotes chromatin opening in vitro. This region also promotes chromatin opening in early mouse embryos and is required for normal development. |
| Audience | Academic |
| Author | Roder, Heinrich Santisteban, Pilar Zaret, Kenneth S. Cuesta, Isabel Donahue, Greg Takenaka, Naomi Osipovich, Anna B. Magnuson, Mark A. Seeholzer, Steven H. Iwafuchi, Makiko |
| AuthorAffiliation | 2 Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid, Spain 1 Institute for Regenerative Medicine, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA 7 Present address: Division of Developmental Biology, Center for Stem Cell & Organoid Medicine, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA 5 Children’s Hospital of Philadelphia, Philadelphia, PA, USA 3 Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA, USA 6 Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain 4 Department of Molecular Physiology and Biophysics and Center for Stem Cell Biology, Vanderbilt University, Nashville, TN, USA |
| AuthorAffiliation_xml | – name: 3 Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA, USA – name: 2 Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid, Spain – name: 5 Children’s Hospital of Philadelphia, Philadelphia, PA, USA – name: 7 Present address: Division of Developmental Biology, Center for Stem Cell & Organoid Medicine, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA – name: 4 Department of Molecular Physiology and Biophysics and Center for Stem Cell Biology, Vanderbilt University, Nashville, TN, USA – name: 6 Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain – name: 1 Institute for Regenerative Medicine, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA |
| Author_xml | – sequence: 1 givenname: Makiko orcidid: 0000-0003-1291-6246 surname: Iwafuchi fullname: Iwafuchi, Makiko email: makiko.iwafuchi@cchmc.org organization: Institute for Regenerative Medicine, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Division of Developmental Biology, Center for Stem Cell & Organoid Medicine, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine – sequence: 2 givenname: Isabel surname: Cuesta fullname: Cuesta, Isabel organization: Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid – sequence: 3 givenname: Greg surname: Donahue fullname: Donahue, Greg organization: Institute for Regenerative Medicine, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania – sequence: 4 givenname: Naomi surname: Takenaka fullname: Takenaka, Naomi organization: Institute for Regenerative Medicine, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania – sequence: 5 givenname: Anna B. surname: Osipovich fullname: Osipovich, Anna B. organization: Department of Molecular Physiology and Biophysics and Center for Stem Cell Biology, Vanderbilt University – sequence: 6 givenname: Mark A. surname: Magnuson fullname: Magnuson, Mark A. organization: Department of Molecular Physiology and Biophysics and Center for Stem Cell Biology, Vanderbilt University – sequence: 7 givenname: Heinrich orcidid: 0000-0003-1860-2491 surname: Roder fullname: Roder, Heinrich organization: Molecular Therapeutics, Fox Chase Cancer Center – sequence: 8 givenname: Steven H. surname: Seeholzer fullname: Seeholzer, Steven H. organization: Children’s Hospital of Philadelphia – sequence: 9 givenname: Pilar surname: Santisteban fullname: Santisteban, Pilar organization: Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Centro de Investigación Biomédica en Red de Cáncer, Instituto de Salud Carlos III – sequence: 10 givenname: Kenneth S. orcidid: 0000-0001-8932-3145 surname: Zaret fullname: Zaret, Kenneth S. email: zaret@pennmedicine.upenn.edu organization: Institute for Regenerative Medicine, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32203463$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceptualization: K.S.Z., M.I., I.C. Experiments: M.I, I.C., N.T., G.D., A.O., H.R., S.S., and P.S. Bioinformatic analysis: M.I and G.D. Writing: M.I., I.C., and K.S.Z. Supervision: K.S.Z and M.A.M. Funding acquisition: K.S.Z. Author contributions |
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| Title | Gene network transitions in embryos depend upon interactions between a pioneer transcription factor and core histones |
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