CORRECTION article

Front. Cell. Infect. Microbiol., 14 August 2017

Sec. Bacteria and Host

Volume 7 - 2017 | https://doi.org/10.3389/fcimb.2017.00364

Corrigendum: Heterogeneous Family of Cyclomodulins: Smart Weapons That Allow Bacteria to Hijack the Eukaryotic Cell Cycle and Promote Infections

  • 1. STLO, Agrocampus Ouest Rennes, Institut National de la Recherche Agronomique Rennes, France

  • 2. Departamento de Biologia Geral, Laboratório de Genética Celular e Molecular, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais Belo Horizonte, Brazil

  • 3. HistoPathologie et Modèles Animaux/Pathogénie des Toxi-Infections Bactériennes, Institut Pasteur Paris, France

  • 4. CHU Purpan USC INRA 1360-CPTP, U1043 Institut National de la Santé et de la Recherche Médicale, Pathogénie Moléculaire et Cellulaire des Infections à Escherichia coli Toulouse, France

  • 5. International Center for Infectiology Research Lyon, France

  • 6. Centre National de la Recherche Scientifique, UMR5308, Institut National de la Santé et de la Recherche Médicale U1111, Ecole Normale Supérieure de Lyon, Université Lyon 1 Lyon, France

  • 7. Département de Biologie, Institut des Agents Infectieux, Hospices Civils de Lyon Lyon, France

In the original article, there was a mistake in the legend for Figure 3 as published.

It was written: Adenylate cyclase toxin (ACT) binds to an unknown receptor at the cell surface through the pentameric subunit (purple), and the catalytic subunit (brown) is translocated to the cytosol.

The correct legend appears below.

ACT is translocated into the cell cytosol either via binding to the αmβ2 integrin as a cell receptor or by direct translocation to the eukaryotic cells cytosol.

Similarly, there were mistakes in Table 1 as published.

It was indicated

Adenylate Cyclase Toxin (ACT)AB5 toxinB. pertussisS1 enzymatic A subunit S2 to S5 binding B subunitsA subunit: acetyltransferase

Enzymatic activity of CNF-1 was indicated as deaminase instead of deamidase.

The corrected Table 1 appears below.

Table 1

Toxin typeSpeciesProteinsEnzymatic activityCell cycle phase delay
PROTEIN OR PEPTIDES TOXINS
Cyclomodulins with enzymatic activities
Cycle Inhibiting Factor (CIF)Cysteine proteaseE. coli (EHEC, EPEC)2 domains: N-terminal (secretion andDeamidaseG1/S
translocation) C-terminal (enzymatic)G2/M
Y. pseudotuberculosis
Pseudomonas sp.
Enterobacter sp.
Serratia sp.
γ-glutamyl transpeptidase (GGT)EnzymeH. pylori1 protein with 2 chains cleaved by autocatalysisGamma-glutamyltransferaseG1/S
Cytolethal Distending Toxin (CDT)Three globular subunitsE. colCdtB catalytic subunit CdtA and CdtC bindingCdtB subunit: DNase andG1/S
subunitsphosphataseG2/M
H. hepaticus
S. enterica serovar Typhimurium
Shiga toxin (Stx) (Verotoxin)AB5 toxinS. dysenteriae E. coli (STEC)stxA enzymatic subunit StxB binding subunitA subunit: N-glycosidaseS
Subtilase AB (SubAB)AB5 toxinE. coli (STEC)SubA enzymatic subunit SubB binding subunitA subunit: proteaseG1/S
Anthrax toxin (Edema toxin / Lethal toxin)Tripartite toxinB. anthracisEdema and/or Lethal factor (A enzymatic subunit) Protective Antigen (B binding subunit)Edema factor: adenylate cyclase Lethal factor: zinc metalloproteaseG1/S
Cholera toxin (Ctx)AB5 toxin Oligomeric complexV. choleraeCTA (enzymatic subunit) comprises CTA1 and CTA2 domains CTB (B binding subunit)ADP-ribosyltransferaseG1/S
Adenylate Cyclase Toxin (ACT)RTX family of toxinB. pertussis2 domains: N- terminal (enzymatic) C-terminal (pore-forming)Adenylate cyclaseG1/S
Vacuolating cytotoxin (VacA)Pore-forming toxinH. pylori3 domains (p33, p55, β-barrel)HypotheticallyG1/S
Cytotoxic Necrotizing Factor 1 (CNF1)Non canonical AB toxinE. coli3 domains: N-terminal (binding) C-terminal (enzymatic) Central (translocation)DeamidaseG2/M
Cyclomodulins without enzymatic activities
Panton–Valentine leukocidin (PVL)β-pore-forming toxin Bi-component toxinS. aureusLukS-PV LukF-PVNoG0/G1
Phenol soluble modulins (PSMs)PeptidesS. aureusPSMα, PSMβ, PSMγNoG2/M
NON-PROTEINACEOUS CYCLOMODULINS
MycolactoneMacrolideM. ulceransNoG0/G1

Cyclomodulins and their key features.

Finally, it was written that “Similar to B. anthracis, B. pertussis produces an adenylate cyclase toxin (ACT), which belongs to the AB5 toxin family (Figure 3) (Melvin et al., 2014).”

A correction has been made to section Cyclomodulins: Protein Toxins or Peptide Toxins, subsection Cyclomodulins with Enzymatic Activities, sub-subsection Adenylate cyclase toxin, first paragraph. The corrected paragraph appears below:

Bordetella pertussis, a Gram-negative bacterial pathogen, is responsible for respiratory infections manifested by whooping cough, with possible lethal complications (Table 1).

Similar to B. anthracis, B. pertussis produces an adenylate cyclase toxin (ACT) (Figure 3) (Melvin et al., 2014). ACT of B. pertussis is a ~200 kDa protein consisting of two functional domains: an N- terminal adenylate cyclase enzyme domain (AC domain) and a pore-forming or hemolysin domain (Hly domain), which belongs to the RTX (Repeats in Toxin) family (Carbonetti, 2010). ACT displays the hemolytic/pore-forming activity along with the adenylate cyclase enzymatic activity (Basler et al., 2006). ACT is released by the Type I bacterial secretion system (Glaser et al., 1988). The Hly domain is required for the delivery of the AC domain into the cell cytosol either via binding to the αmβ2 integrin (CD11b/CD18) as a cell receptor or by direct translocation to the eukaryotic cells cytosol (Guermonprez et al., 2001; Eby et al., 2010).

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way.

Statements

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

  • 1

    BaslerM.MasinJ.OsickaR.SeboP. (2006). Pore-forming and enzymatic activities of Bordetella pertussis adenylate cyclase toxin synergize in promoting lysis of monocytes. Infect. Immun. 74, 22072214. 10.1128/IAI.74.4.2207-2214.2006

  • 2

    CarbonettiN. H. (2010). Pertussis toxin and adenylate cyclase toxin: key virulence factors of Bordetella pertussis and cell biology tools. Future Microbiol. 5, 455469. 10.2217/fmb.09.133

  • 3

    EbyJ. C.CieslaW. P.HammanW.DonatoG. M.PicklesR. J.HewlettE. L.et al. (2010). Selective Translocation of the Bordetella pertussis adenylate cyclase toxin across the basolateral membranes of polarized epithelial cells. J. Biol. Chem.285, 1066210670. 10.1074/jbc.M109.089219

  • 4

    GlaserP.SakamotoH.BellalouJ.UllmannA.DanchinA. (1988). Secretion of cyclolysin, the calmodulin-sensitive adenylate cyclase-haemolysin bifunctional protein of Bordetella pertussis. EMBO J.7, 39974004.

  • 5

    GuermonprezP.KhelefN.BlouinE.RieuP.Ricciardi-CastagnoliP.GuisoN.et al. (2001). The adenylate cyclase toxin of Bordetella pertussis binds to target cells via the αMβ2gf integrin (CD11b/CD18). J. Exp. Med.193, 10351044. 10.1084/jem.193.9.1035

  • 6

    MelvinJ. A.SchellerE. V.MillerJ. F.CotterP. A. (2014). Bordetella pertussis pathogenesis: current and future challenges. Nat. Rev. Microbiol.12, 274288. 10.1038/nrmicro3235

Summary

Keywords

eukaryotic cell cycle alteration, bacterial toxins, cyclomodulins, colonization, invasion, infective efficiency, reduced host response

Citation

El-Aouar Filho RA, Nicolas A, De Paula Castro TL, Deplanche M, De Carvalho Azevedo VA, Goossens PL, Taieb F, Lina G, Le Loir Y and Berkova N (2017) Corrigendum: Heterogeneous Family of Cyclomodulins: Smart Weapons That Allow Bacteria to Hijack the Eukaryotic Cell Cycle and Promote Infections. Front. Cell. Infect. Microbiol. 7:364. doi: 10.3389/fcimb.2017.00364

Received

20 July 2017

Accepted

28 July 2017

Published

14 August 2017

Volume

7 - 2017

Edited and reviewed by

Georgios N. Belibasakis, Karolinska Institute (KI), Sweden

Updates

Copyright

*Correspondence: Nadia Berkova

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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