Structural basis for TBP displacement from TATA box DNA by the Swi2/Snf2 ATPase Mot1.


Journal

Nature structural & molecular biology
ISSN: 1545-9985
Titre abrégé: Nat Struct Mol Biol
Pays: United States
ID NLM: 101186374

Informations de publication

Date de publication:
05 2023
Historique:
received: 22 03 2022
accepted: 13 03 2023
medline: 19 5 2023
pubmed: 28 4 2023
entrez: 27 4 2023
Statut: ppublish

Résumé

The Swi2/Snf2 family transcription regulator Modifier of Transcription 1 (Mot1) uses adenosine triphosphate (ATP) to dissociate and reallocate the TATA box-binding protein (TBP) from and between promoters. To reveal how Mot1 removes TBP from TATA box DNA, we determined cryogenic electron microscopy structures that capture different states of the remodeling reaction. The resulting molecular video reveals how Mot1 dissociates TBP in a process that, intriguingly, does not require DNA groove tracking. Instead, the motor grips DNA in the presence of ATP and swings back after ATP hydrolysis, moving TBP to a thermodynamically less stable position on DNA. Dislodged TBP is trapped by a chaperone element that blocks TBP's DNA binding site. Our results show how Swi2/Snf2 proteins can remodel protein-DNA complexes through DNA bending without processive DNA tracking and reveal mechanistic similarities to RNA gripping DEAD box helicases and RIG-I-like immune sensors.

Identifiants

pubmed: 37106137
doi: 10.1038/s41594-023-00966-0
pii: 10.1038/s41594-023-00966-0
doi:

Substances chimiques

Adenosine Triphosphatases EC 3.6.1.-
Transcription Factors 0
TATA-Box Binding Protein 0
Saccharomyces cerevisiae Proteins 0
DNA 9007-49-2
Adenosine Triphosphate 8L70Q75FXE
TATA-Binding Protein Associated Factors 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

640-649

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature America, Inc.

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Auteurs

Stephan Woike (S)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.

Sebastian Eustermann (S)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.
European Molecular Biology Laboratory (EMBL), Structural and Computational Biology Unit, Heidelberg, Germany.

James Jung (J)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.
Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Queensland, Australia.

Simon Josef Wenzl (SJ)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.

Götz Hagemann (G)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.

Joseph Bartho (J)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.

Katja Lammens (K)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.

Agata Butryn (A)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.
Macromolecular Machines Laboratory, Francis Crick Institute, London, UK.

Franz Herzog (F)

Gene Center, Ludwig-Maximilians-Universität, Munich, Germany.
Institute Krems Bioanalytics, IMC University of Applied Sciences, Krems, Austria.

Karl-Peter Hopfner (KP)

Department of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany. hopfner@genzentrum.lmu.de.
Gene Center, Ludwig-Maximilians-Universität, Munich, Germany. hopfner@genzentrum.lmu.de.

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