Polyelectrolyte interactions enable rapid association and dissociation in high-affinity disordered protein complexes.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
12 11 2020
Historique:
received: 21 07 2020
accepted: 14 09 2020
entrez: 13 11 2020
pubmed: 14 11 2020
medline: 1 12 2020
Statut: epublish

Résumé

Highly charged intrinsically disordered proteins can form complexes with very high affinity in which both binding partners fully retain their disorder and dynamics, exemplified by the positively charged linker histone H1.0 and its chaperone, the negatively charged prothymosin α. Their interaction exhibits another surprising feature: The association/dissociation kinetics switch from slow two-state-like exchange at low protein concentrations to fast exchange at higher, physiologically relevant concentrations. Here we show that this change in mechanism can be explained by the formation of transient ternary complexes favored at high protein concentrations that accelerate the exchange between bound and unbound populations by orders of magnitude. Molecular simulations show how the extreme disorder in such polyelectrolyte complexes facilitates (i) diffusion-limited binding, (ii) transient ternary complex formation, and (iii) fast exchange of monomers by competitive substitution, which together enable rapid kinetics. Biological polyelectrolytes thus have the potential to keep regulatory networks highly responsive even for interactions with extremely high affinities.

Identifiants

pubmed: 33184256
doi: 10.1038/s41467-020-18859-x
pii: 10.1038/s41467-020-18859-x
pmc: PMC7661507
doi:

Substances chimiques

Intrinsically Disordered Proteins 0
Molecular Chaperones 0
Polyelectrolytes 0
Protein Precursors 0
prothymosin alpha 0
Thymosin 61512-21-8

Types de publication

Journal Article Research Support, N.I.H., Intramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

5736

Commentaires et corrections

Type : ErratumIn

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Auteurs

Andrea Sottini (A)

Department of Biochemistry, University of Zurich, Zurich, Switzerland.

Alessandro Borgia (A)

Department of Biochemistry, University of Zurich, Zurich, Switzerland.
Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.

Madeleine B Borgia (MB)

Department of Biochemistry, University of Zurich, Zurich, Switzerland.
Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.

Katrine Bugge (K)

Structural Biology and NMR Laboratory (SBiNLab) and REPIN, Department of Biology, Ole Maaloes Vej 5, University of Copenhagen, 2200, Copenhagen, Denmark.

Daniel Nettels (D)

Department of Biochemistry, University of Zurich, Zurich, Switzerland.

Aritra Chowdhury (A)

Department of Biochemistry, University of Zurich, Zurich, Switzerland.

Pétur O Heidarsson (PO)

Department of Biochemistry, University of Zurich, Zurich, Switzerland.
Department of Biochemistry, Science Institute, University of Iceland, Dunhagi 3, 107, Reykjavík, Iceland.

Franziska Zosel (F)

Department of Biochemistry, University of Zurich, Zurich, Switzerland.
Novo Nordisk A/S, Novo Nordisk Park, 2760, Måløv, Denmark.

Robert B Best (RB)

Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892-0520, USA. robert.best2@nih.gov.

Birthe B Kragelund (BB)

Structural Biology and NMR Laboratory (SBiNLab) and REPIN, Department of Biology, Ole Maaloes Vej 5, University of Copenhagen, 2200, Copenhagen, Denmark. bbk@bio.ku.dk.

Benjamin Schuler (B)

Department of Biochemistry, University of Zurich, Zurich, Switzerland. schuler@bioc.uzh.ch.
Department of Physics, University of Zurich, Zurich, Switzerland. schuler@bioc.uzh.ch.

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Classifications MeSH