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Protein kinase B controls Mycobacterium tuberculosis growth via phosphorylation of the transcriptional regulator Lsr2 at threonine 112

Authors
  • Alqaseer, Kawther1, 2
  • Turapov, Obolbek1
  • Barthe, Philippe3
  • Jagatia, Heena4
  • De Visch, Angélique3
  • Roumestand, Christian3
  • Wegrzyn, Malgorzata1
  • Bartek, Iona L.5
  • Voskuil, Martin I.5
  • O'Hare, Helen M.1, 1
  • Ajuh, Paul6
  • Bottrill, Andrew R.1
  • Witney, Adam A.7
  • Cohen‐Gonsaud, Martin3
  • Waddell, Simon J.4
  • Mukamolova, Galina V.1
  • 1 University of Leicester, UK , (United Kingdom)
  • 2 Najaf Governorate, Iraq , (Iraq)
  • 3 University of Montpellier, France , (France)
  • 4 University of Sussex, UK , (United Kingdom)
  • 5 University of Colorado School of Medicine, USA , (United States)
  • 6 Liverpool Science Park, UK , (United Kingdom)
  • 7 St George's University of London, UK , (United Kingdom)
Type
Published Article
Journal
Molecular Microbiology
Publisher
Wiley (Blackwell Publishing)
Publication Date
Oct 10, 2019
Volume
112
Issue
6
Pages
1847–1862
Identifiers
DOI: 10.1111/mmi.14398
PMID: 31562654
PMCID: PMC6906086
Source
PubMed Central
License
Unknown
External links

Abstract

Protein kinase B (PknB) is essential for growth of Mycobacterium tuberculosis because of its central role in regulation of peptidoglycan biosynthesis. Here we describe that PknB, controls activation of alternative pathways that are not required for active growth but crucial for survival in stressful environment and virulence. PknB phosphorylates Lsr2, a global transcriptional regulator, at threonine 112 and controls its binding to DNA and transcription of target genes.

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