Literature DB >> 15735309

Energetics of structural transitions of the addiction antitoxin MazE: is a programmed bacterial cell death dependent on the intrinsically flexible nature of the antitoxins?

Jurij Lah1, Mario Simic, Gorazd Vesnaver, Irina Marianovsky, Gad Glaser, Hanna Engelberg-Kulka, Remy Loris.   

Abstract

The Escherichia coli mazEF addiction module plays a crucial role in the cell death program that is triggered under various stress conditions. It codes for the toxin MazF and the antitoxin MazE, which interferes with the lethal action of the toxin. To better understand the role of various conformations of MazE in bacterial life, its order-disorder transitions were monitored by differential scanning calorimetry, spectropolarimetry, and fluorimetry. The changes in spectral and thermodynamic properties accompanying MazE dimer denaturation can be described in terms of a compensating reversible process of the partial folding of the unstructured C-terminal half (high mean net charge, low mean hydrophobicity) and monomerization coupled with the partial unfolding of the structured N-terminal half (low mean net charge, high mean hydrophobicity). At pH<or=4.5 and T<50 degrees C, the unstructured polypeptide chains of the MazE dimer fold into (pre)molten globule-like conformations that thermally stabilize the dimeric form of the protein. The simulation based on the thermodynamic and structural information on various addiction modules suggests that both the conformational adaptability of the dimeric antitoxin form (binding to the toxins and DNA) and the reversible transformation to the more flexible monomeric form are essential for the regulation of bacterial cell life and death.

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Year:  2005        PMID: 15735309     DOI: 10.1074/jbc.M501128200

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  11 in total

1.  Driving forces of gyrase recognition by the addiction toxin CcdB.

Authors:  Mario Simic; Natalie De Jonge; Remy Loris; Gorazd Vesnaver; Jurij Lah
Journal:  J Biol Chem       Date:  2009-05-22       Impact factor: 5.157

2.  Molecular mechanisms of multiple toxin-antitoxin systems are coordinated to govern the persister phenotype.

Authors:  Rick A Fasani; Michael A Savageau
Journal:  Proc Natl Acad Sci U S A       Date:  2013-06-18       Impact factor: 11.205

3.  Structural and thermodynamic characterization of Vibrio fischeri CcdB.

Authors:  Natalie De Jonge; Walter Hohlweg; Abel Garcia-Pino; Michal Respondek; Lieven Buts; Sarah Haesaerts; Jurij Lah; Klaus Zangger; Remy Loris
Journal:  J Biol Chem       Date:  2009-12-02       Impact factor: 5.157

4.  Expanding the proteome: disordered and alternatively folded proteins.

Authors:  H Jane Dyson
Journal:  Q Rev Biophys       Date:  2011-07-01       Impact factor: 5.318

5.  Toxin-antitoxin systems are ubiquitous and plasmid-encoded in vancomycin-resistant enterococci.

Authors:  Elizabeth M Moritz; Paul J Hergenrother
Journal:  Proc Natl Acad Sci U S A       Date:  2006-12-26       Impact factor: 11.205

6.  Functional insights into the Streptococcus pneumoniae HicBA toxin-antitoxin system based on a structural study.

Authors:  Do-Hee Kim; Sung-Min Kang; Sung Jean Park; Chenglong Jin; Hye-Jin Yoon; Bong-Jin Lee
Journal:  Nucleic Acids Res       Date:  2018-07-06       Impact factor: 16.971

7.  DNA duplex stability: the role of preorganized electrostatics.

Authors:  Urban Bren; Jurij Lah; Matevz Bren; Václav Martínek; Jan Florián
Journal:  J Phys Chem B       Date:  2010-03-04       Impact factor: 2.991

8.  Regulation of Escherichia coli SOS mutagenesis by dimeric intrinsically disordered umuD gene products.

Authors:  S M Simon; F J R Sousa; R Mohana-Borges; G C Walker
Journal:  Proc Natl Acad Sci U S A       Date:  2008-01-23       Impact factor: 11.205

9.  Unrelated toxin-antitoxin systems cooperate to induce persistence.

Authors:  Rick A Fasani; Michael A Savageau
Journal:  J R Soc Interface       Date:  2015-07-06       Impact factor: 4.118

10.  RelB and RelE of Escherichia coli form a tight complex that represses transcription via the ribbon-helix-helix motif in RelB.

Authors:  Martin Overgaard; Jonas Borch; Kenn Gerdes
Journal:  J Mol Biol       Date:  2009-09-08       Impact factor: 5.469

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