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X-Ray Structure of the Arenavirus Glycoprotein GP2 in Its Postfusion Hairpin Conformation

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X-Ray Structure of the Arenavirus Glycoprotein GP2 in Its Postfusion Hairpin Conformation Corrections NEUROBIOLOGY Correction for “High-resolution structure of hair-cell tip links,” The authors note that Figure 3 appeared incorrectly. The by Bechara Kachar, Marianne Parakkal, Mauricio Kurc, Yi-dong corrected figure and its legend appear below. This error does not Zhao, and Peter G. Gillespie, which appeared in issue 24, affect the conclusions of the article. November 21, 2000, of Proc Natl Acad Sci USA (97:13336– 13341; 10.1073/pnas.97.24.13336). CORRECTIONS Fig. 3. Upper and lower attachments of the tip link. (A and B) Freeze-etch images of tip-link upper insertions in guinea pig cochlea (A) and (left to right) two from guinea pig cochlea, two from bullfrog sacculus, and two from guinea pig utriculus (B). Each example shows pronounced branching. (C and D) Freeze- etch images of the tip-link lower insertion in stereocilia from bullfrog sacculus (C) and guinea pig utriculus (D); multiple strands (arrows) arise from the stereociliary tip. (E) Freeze-fracture image of stereociliary tips from bullfrog sacculus; indentations at tips are indicated by arrows. (Scale bars: A = 100 nm, B = 25 nm; C–E = 100 nm.) www.pnas.org/cgi/doi/10.1073/pnas.1311228110 www.pnas.org PNAS | July 16, 2013 | vol. 110 | no. 29 | 12155–12156 Downloaded by guest on September 28, 2021 BIOCHEMISTRY BIOPHYSICS AND COMPUTATIONAL BIOLOGY, STATISTICS Correction for “X-ray structure of the arenavirus glycoprotein Correction for “Differential principal component analysis of GP2 in its postfusion hairpin conformation,” by Sébastien Igo- ChIP-seq,” by Hongkai Ji, Xia Li, Qian-fei Wang, and Yang net, Marie-Christine Vaney, Clemens Vonhrein, Gérard Bri- Ning, which appeared in issue 17, April 23, 2013, of Proc Natl cogne, Enrico A. Stura, Hans Hengartner, Bruno Eschli, and Acad Sci USA (110:6789–6794; first published April 8, 2013; Félix A. Rey, which appeared in issue 50, December 13, 2011, 10.1073/pnas.1204398110). of Proc Natl Acad Sci USA (108:19967–19972; first published The authors note the following statement should be added to November 28, 2011; 10.1073/pnas.1108910108). the Acknowledgments: “Q.-f.W. is supported by the Strategic The authors note that, due to a printer’s error, the author Priority Research Program of the Chinese Academy of Sciences name Clemens Vonhrein should instead appear as Clemens (Grant No. XDA01010305).” Vonrhein. The corrected author line appears below. The online version has been corrected. www.pnas.org/cgi/doi/10.1073/pnas.1311614110 Sébastien Igonet, Marie-Christine Vaney, Clemens Vonrhein, Gérard Bricogne, Enrico A. Stura, Hans Hengartner, Bruno Eschli, and Félix A. Rey www.pnas.org/cgi/doi/10.1073/pnas.1311209110 12156 | www.pnas.org Downloaded by guest on September 28, 2021 X-ray structure of the arenavirus glycoprotein GP2 in its postfusion hairpin conformation Sébastien Igoneta,b, Marie-Christine Vaneya,b, Clemens Vonrheinc, Gérard Bricognec, Enrico A. Sturad, Hans Hengartnere, Bruno Eschlie, and Félix A. Reya,b,1 aDépartement de Virologie, Unité de Virologie Structurale, Institut Pasteur, F-75724 Paris Cedex 15, France; bCentre National de la Recherche Scientifique, Unité de Recherche Associée 3015, F-75724 Paris Cedex 15, France; cGlobal Phasing Ltd., Cambridge CB3 0AX, United Kingdom; dCommissariat à l’Energie Atomique Saclay, Service d’Ingénierie et d’Etudes des Protéines, CE-Saclay F-91191 Gif-sur-Yvette Cedex, France; and eInstitute of Experimental Immunology, University Hospital, CH 8557 Zürich, Switzerland Edited by Robert A. Lamb, Northwestern University, Evanston, IL, and approved October 10, 2011 (received for review June 19, 2011) Arenaviruses are important agents of zoonotic disease worldwide. peptide (SSP, aa 1–58), the surface exposed GP1 (aa 59–265), The virions expose a tripartite envelope glycoprotein complex at and the transmembrane GP2 (266–498) to make a ðSSP∕GP1∕ their surface, formed by the glycoprotein subunits GP1, GP2 and GP2Þ3 trimeric complex. SSP is myristoylated (9) and rearranges the stable signal peptide. This complex is responsible for binding after signalase cleavage to translocate its C-terminal end back to to target cells and for the subsequent fusion of viral and host-cell the cytosolic side of the membrane, thus traversing the membrane membranes for entry. During this process, the acidic environment twice (10). Its interactions with the cytosolic domain of GP2 of the endosome triggers a fusogenic conformational change in are responsible for SSP retention as part of the mature GPC, the transmembrane GP2 subunit of the complex. We report here as shown for Junin virus (11). GP1 and GP2 are proteolytically the crystal structure of the recombinant GP2 ectodomain of the derived from the GPC ectodomain by subtilase SKI-1/S1P lymphocytic choriomeningitis virus, the arenavirus type species, (Fig. 1A) in the early Golgi compartments. This cleavage event at 1.8-Å resolution. The structure shows the characteristic trimeric is essential for productive infection and viral spread (12–15). GP1 coiled coil present in class I viral fusion proteins, with a central stut- is responsible for interactions with cellular receptors for entry. ter that allows a close structural alignment with most of the avail- Old World arenaviruses such as LCMV or Lassa fever virus use able structures of class I and III viral fusion proteins. The structure α-dystroglycan as entry receptor (16, 17), whereas the pathogenic further shows a number of intrachain salt bridges stabilizing the subgroup of New World arenaviruses uses the transferrin recep- postfusion hairpin conformation, one of which involves an aspartic tor-1 (TfR1) (18, 19). The interaction of GP1 with the receptor acid that appears released from a critical interaction with the stable results in virion uptake by the cell into an endosomal compart- signal peptide upon low pH activation. ment, the acidic environment of which triggers a fusogenic con- formational change in GP2 (20), the membrane fusion subunit. enveloped viruses ∣ membrane fusion ∣ RNA viruses ∣ emerging viruses GP2 contains a bipartite fusion peptide, with one of the segments located at the very N terminus of the protein, as observed in many BIOCHEMISTRY renaviruses are agents of emerging zoonotic diseases such as class I viral fusion proteins. GP2 also has a disulfide-bond- severe hemorrhagic fever. They cause chronic infections in A stabilized internal fusion loop located close to the N terminus rodents, the natural hosts, and transmission to humans often oc- (21), similar to the Ebola virus (22) and the avian sarcoma/ curs as a result of man-driven changes in the ecosystem that alter leucosis retrovirus fusion proteins (23). For Junin virus—and by the rodent population. Examples of recently emerged arenavirus extension, for all arenaviruses—the acid sensitivity was shown to infections in humans are those of Chapare and Lujo hemorrhagic fever viruses in Bolivia and South Africa, respectively (1, 2). be controlled, at least in part, by interactions between the GP2 The Arenaviridae family contains a single genus subdivided in ectodomain and the luminal loop connecting the two transmem- two separate serological groups, the Old World and the New brane (TM) segments of SSP (24). World arenaviruses. The lymphocytic choriomeningitis virus Amino acid sequence analyses and biochemical studies with (LCMV), Lujo virus, and the highly pathogenic Lassa fever virus, recombinant fragments have indicated that, despite the presence which is endemic of West Africa, are members of the first group. of a bipartite fusion loop, GP2 is a typical class I fusion protein, The second one includes several South American hemorrhagic forming an alpha helix-rich trimer in its postfusion state (25). α fever viruses—among them Machupo, Junin, Sabia, Guanarito, These studies identified two -helical regions (N- and C-term- and Chapare viruses. LCMV is the arenavirus type species and inal) with a heptad repeat pattern in the N-terminal helix (25, 26). is widely used as experimental model for the study of viral per- A loop containing a conserved disulfide bond connects the two sistence and pathogenesis (3). LCMV infections in humans occur helices. A model of the structure has been proposed by compar- worldwide, and, although often asymptomatic, they can cause a ison with the GP2 counterpart from Ebola virus (26), for which spectrum of illnesses ranging from isolated fever to meningitis the structure is known (27, 28). Ebola virus, however, belongs to a and encephalitis (4, 5). In particular, a number of fatal cases different viral family (the Filoviridae), and other than the pre- of transplant-associated LCMV infections have been recently sence of the characteristic heptad repeat pattern typical of coiled reported, illustrating the threat to patients undergoing immuno- suppressive treatment (6–8). Author contributions: B.E. and F.A.R. designed research; S.I. and M.-C.V. performed Arenavirus virions are pleomorphic enveloped particles con- research; H.H. and B.E. contributed new reagents/analytic tools; S.I., M.-C.V., C.V., G.B., taining a bisegmented, ambisense RNA genome with four open E.A.S., and F.A.R. analyzed data; and S.I. and F.A.R. wrote the paper. reading frames. The long (L) RNA segment encodes the viral The authors declare no conflict of interest. RNA-dependent RNA polymerase (protein L, 200 kDa) and a This article is a PNAS Direct Submission. small RING-finger protein (Z, 11 kDa) involved viral replication. Data deposition: Coordinates and structure factors have been deposited in the Protein The short (S) segment encodes the nucleoprotein (NP, 63 kDa) Data Bank, www.pdb.org (PDB ID code 3MKO). and the viral glycoprotein complex precursor (GPC, 75 kDa). 1To whom correspondence should be addressed. E-mail: [email protected]. Proteolytic maturation of the 498-amino acid GPC precursor This article contains supporting information online at www.pnas.org/lookup/suppl/ results in three noncovalently bound subunits: the stable signal doi:10.1073/pnas.1108910108/-/DCSupplemental.
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