Conformational plasticity of the ClpAP AAA+ protease couples protein unfolding and proteolysis.


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 2020
Historique:
received: 22 10 2019
accepted: 09 03 2020
pubmed: 22 4 2020
medline: 2 10 2020
entrez: 22 4 2020
Statut: ppublish

Résumé

The ClpAP complex is a conserved bacterial protease that unfolds and degrades proteins targeted for destruction. The ClpA double-ring hexamer powers substrate unfolding and translocation into the ClpP proteolytic chamber. Here, we determined high-resolution structures of wild-type Escherichia coli ClpAP undergoing active substrate unfolding and proteolysis. A spiral of pore loop-substrate contacts spans both ClpA AAA+ domains. Protomers at the spiral seam undergo nucleotide-specific rearrangements, supporting substrate translocation. IGL loops extend flexibly to bind the planar, heptameric ClpP surface with the empty, symmetry-mismatched IGL pocket maintained at the seam. Three different structures identify a binding-pocket switch by the IGL loop of the lowest positioned protomer, involving release and re-engagement with the clockwise pocket. This switch is coupled to a ClpA rotation and a network of conformational changes across the seam, suggesting that ClpA can rotate around the ClpP apical surface during processive steps of translocation and proteolysis.

Identifiants

pubmed: 32313240
doi: 10.1038/s41594-020-0409-5
pii: 10.1038/s41594-020-0409-5
pmc: PMC7529148
mid: NIHMS1625877
doi:

Substances chimiques

Escherichia coli Proteins 0
Multiprotein Complexes 0
Trans-Activators 0
replication initiator protein 0
adenosine 5'-O-(3-thiotriphosphate) 35094-46-3
Adenosine Triphosphate 8L70Q75FXE
ClpA protease, E coli EC 3.4.21.53
ClpP protease, E coli EC 3.4.21.92
Endopeptidase Clp EC 3.4.21.92
DNA Helicases EC 3.6.4.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Video-Audio Media

Langues

eng

Sous-ensembles de citation

IM

Pagination

406-416

Subventions

Organisme : NIGMS NIH HHS
ID : R01 GM099836
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM110001
Pays : United States
Organisme : NIBIB NIH HHS
ID : T32 EB009383
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM008284
Pays : United States

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Auteurs

Kyle E Lopez (KE)

Graduate Program in Biophysics, University of California, San Francisco, San Francisco, CA, USA.
Department of Biochemistry and Biophysics, Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, USA.

Alexandrea N Rizo (AN)

Department of Biochemistry and Biophysics, Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, USA.
Graduate Program in Chemical Biology, University of Michigan, Ann Arbor, MI, USA.

Eric Tse (E)

Department of Biochemistry and Biophysics, Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, USA.

JiaBei Lin (J)

Department of Biochemistry and Biophysics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.

Nathaniel W Scull (NW)

Department of Chemistry, The University of Alabama at Birmingham, Birmingham, AL, USA.

Aye C Thwin (AC)

Department of Biochemistry and Biophysics, Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, USA.

Aaron L Lucius (AL)

Department of Chemistry, The University of Alabama at Birmingham, Birmingham, AL, USA.

James Shorter (J)

Department of Biochemistry and Biophysics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.

Daniel R Southworth (DR)

Department of Biochemistry and Biophysics, Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, USA. daniel.southworth@ucsf.edu.

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