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The lytic transglycosylase MltB connects membrane homeostasis and in vivo fitness of Acinetobacter baumannii
Author(s) -
Crépin Sébastien,
Ottosen Elizabeth N.,
Peters Katharina,
Smith Sara N.,
Himpsl Stephanie D.,
Vollmer Waldemar,
Mobley Harry L. T.
Publication year - 2018
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.14000
Subject(s) - acinetobacter baumannii , biology , microbiology and biotechnology , virulence , regulon , pilus , lytic cycle , peptidoglycan , gene , genetics , mutant , bacteria , pseudomonas aeruginosa , virus
Summary Acinetobacter baumannii has emerged as a leading nosocomial pathogen, infecting a wide range of anatomic sites including the respiratory tract and the bloodstream. In addition to being multi‐drug resistant, little is known about the molecular basis of A. baumannii pathogenesis. To better understand A . baumannii virulence, a combination of a transposon‐sequencing (TraDIS) screen and the neutropenic mouse model of bacteremia was used to identify the full set of fitness genes required during bloodstream infection. The lytic transglycosylase MltB was identified as a critical fitness factor. MltB cleaves the Mur N Ac‐Glc N Ac bond of peptidoglycan, which leads to cell wall remodeling. Here we show that MltB is part of a complex network connecting resistance to stresses, membrane homeostasis, biogenesis of pili and in vivo fitness. Indeed, inactivation of mltB not only impaired resistance to serum complement, cationic antimicrobial peptides and oxygen species, but also altered the cell envelope integrity, activated the envelope stress response, drastically reduced the number of pili at the cell surface and finally, significantly decreased colonization of both the bloodstream and the respiratory tract.