Structures of a deAMPylation complex rationalise the switch between antagonistic catalytic activities of FICD.


Journal

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

Informations de publication

Date de publication:
18 08 2021
Historique:
received: 17 02 2021
accepted: 15 07 2021
entrez: 19 8 2021
pubmed: 20 8 2021
medline: 15 9 2021
Statut: epublish

Résumé

The endoplasmic reticulum (ER) Hsp70 chaperone BiP is regulated by AMPylation, a reversible inactivating post-translational modification. Both BiP AMPylation and deAMPylation are catalysed by a single ER-localised enzyme, FICD. Here we present crystallographic and solution structures of a deAMPylation Michaelis complex formed between mammalian AMPylated BiP and FICD. The latter, via its tetratricopeptide repeat domain, binds a surface that is specific to ATP-state Hsp70 chaperones, explaining the exquisite selectivity of FICD for BiP's ATP-bound conformation both when AMPylating and deAMPylating Thr518. The eukaryotic deAMPylation mechanism thus revealed, rationalises the role of the conserved Fic domain Glu234 as a gatekeeper residue that both inhibits AMPylation and facilitates hydrolytic deAMPylation catalysed by dimeric FICD. These findings point to a monomerisation-induced increase in Glu234 flexibility as the basis of an oligomeric state-dependent switch between FICD's antagonistic activities, despite a similar mode of engagement of its two substrates - unmodified and AMPylated BiP.

Identifiants

pubmed: 34408154
doi: 10.1038/s41467-021-25076-7
pii: 10.1038/s41467-021-25076-7
pmc: PMC8373988
doi:

Substances chimiques

Endoplasmic Reticulum Chaperone BiP 0
Heat-Shock Proteins 0
Membrane Proteins 0
Adenosine Monophosphate 415SHH325A
Adenosine Triphosphate 8L70Q75FXE
FICD protein, human EC 2.7.7.-
Nucleotidyltransferases EC 2.7.7.-

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

5004

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 200848/Z/16/Z
Pays : United Kingdom

Informations de copyright

© 2021. The Author(s).

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Auteurs

Luke A Perera (LA)

Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK. lp397@cam.ac.uk.

Steffen Preissler (S)

Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.

Nathan R Zaccai (NR)

Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.

Sylvain Prévost (S)

Institut Laue-Langevin, Grenoble, France.

Juliette M Devos (JM)

Institut Laue-Langevin, Grenoble, France.

Michael Haertlein (M)

Institut Laue-Langevin, Grenoble, France.

David Ron (D)

Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK. dr360@medschl.cam.ac.uk.

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Classifications MeSH