3O9R

Effector domain of NS1 from influenza A/PR/8/34 containing a W187A mutation


Experimental Data Snapshot

  • Method: X-RAY DIFFRACTION
  • Resolution: 2.00 Å
  • R-Value Free: 0.253 
  • R-Value Work: 0.196 
  • R-Value Observed: 0.199 

wwPDB Validation   3D Report Full Report


This is version 1.2 of the entry. See complete history


Literature

A Transient Homotypic Interaction Model for the Influenza A Virus NS1 Protein Effector Domain.

Kerry, P.S.Ayllon, J.Taylor, M.A.Hass, C.Lewis, A.Garcia-Sastre, A.Randall, R.E.Hale, B.G.Russell, R.J.

(2011) PLoS One 6: e17946-e17946

  • DOI: https://doi.org/10.1371/journal.pone.0017946
  • Primary Citation of Related Structures:  
    3O9Q, 3O9R, 3O9S, 3O9T, 3O9U, 3OA9

  • PubMed Abstract: 

    Influenza A virus NS1 protein is a multifunctional virulence factor consisting of an RNA binding domain (RBD), a short linker, an effector domain (ED), and a C-terminal 'tail'. Although poorly understood, NS1 multimerization may autoregulate its actions. While RBD dimerization seems functionally conserved, two possible apo ED dimers have been proposed (helix-helix and strand-strand). Here, we analyze all available RBD, ED, and full-length NS1 structures, including four novel crystal structures obtained using EDs from divergent human and avian viruses, as well as two forms of a monomeric ED mutant. The data reveal the helix-helix interface as the only strictly conserved ED homodimeric contact. Furthermore, a mutant NS1 unable to form the helix-helix dimer is compromised in its ability to bind dsRNA efficiently, implying that ED multimerization influences RBD activity. Our bioinformatical work also suggests that the helix-helix interface is variable and transient, thereby allowing two ED monomers to twist relative to one another and possibly separate. In this regard, we found a mAb that recognizes NS1 via a residue completely buried within the ED helix-helix interface, and which may help highlight potential different conformational populations of NS1 (putatively termed 'helix-closed' and 'helix-open') in virus-infected cells. 'Helix-closed' conformations appear to enhance dsRNA binding, and 'helix-open' conformations allow otherwise inaccessible interactions with host factors. Our data support a new model of NS1 regulation in which the RBD remains dimeric throughout infection, while the ED switches between several quaternary states in order to expand its functional space. Such a concept may be applicable to other small multifunctional proteins.


  • Organizational Affiliation

    Biomedical Sciences Research Complex, University of St Andrews, St Andrews, Fife, United Kingdom.


Macromolecules
Find similar proteins by:  (by identity cutoff)  |  3D Structure
Entity ID: 1
MoleculeChains Sequence LengthOrganismDetailsImage
Nonstructural protein 1
A, B
152Influenza A virus (A/reassortant/IVR108(Sydney/5/1995 x Puerto Rico/8/1934)(H3N2))Mutation(s): 1 
Gene Names: NS1
UniProt
Find proteins for P03496 (Influenza A virus (strain A/Puerto Rico/8/1934 H1N1))
Explore P03496 
Go to UniProtKB:  P03496
Entity Groups  
Sequence Clusters30% Identity50% Identity70% Identity90% Identity95% Identity100% Identity
UniProt GroupP03496
Sequence Annotations
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  • Reference Sequence
Experimental Data & Validation

Experimental Data

  • Method: X-RAY DIFFRACTION
  • Resolution: 2.00 Å
  • R-Value Free: 0.253 
  • R-Value Work: 0.196 
  • R-Value Observed: 0.199 
  • Space Group: P 21 21 21
Unit Cell:
Length ( Å )Angle ( ˚ )
a = 33.606α = 90
b = 70.109β = 90
c = 104.258γ = 90
Software Package:
Software NamePurpose
PHENIXrefinement

Structure Validation

View Full Validation Report



Entry History 

Deposition Data

Revision History  (Full details and data files)

  • Version 1.0: 2011-05-11
    Type: Initial release
  • Version 1.1: 2011-07-13
    Changes: Version format compliance
  • Version 1.2: 2024-02-21
    Changes: Data collection, Database references