Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0240066 (
iron deficiency
)
7,156
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Acinetobacter baumannii
is one of the major causes of hard to treat multidrug-resistant hospital infections.
A. baumannii
features contributing to its spread and persistence in clinical environment are only beginning to be explored. Bacterial toxin-antitoxin (TA) systems are genetic loci shown to be involved in plasmid maintenance and proposed to function as components of stress response networks. Here we present a thorough characterization of type II system of
A. baumannii
, which is the most ubiquitous TA module present in
A. baumannii
plasmids.
higBA
of
A. baumannii
is a reverse TA (the toxin gene is the first in the operon) and shows little homology to other TA systems of RelE superfamily. It is represented by two variants, which both are functional albeit exhibit strong difference in sequence conservation. The
higBA2
operon is found on ubiquitous 11 Kb pAB120 plasmid, conferring carbapenem resistance to clinical
A. baumannii
isolates and represents a
higBA
variant that can be found with multiple sequence variations. We show here that
higBA2
is capable to confer maintenance of unstable plasmid in
Acinetobacter
species. HigB2 toxin functions as a
ribonuclease
and its activity is neutralized by HigA2 antitoxin through formation of an unusually large heterooligomeric complex. Based on the
in vivo
expression analysis of
gfp
reporter gene we propose that HigA2 antitoxin and HigBA2 protein complex bind the
higBA2
promoter region to downregulate its transcription. We also demonstrate that
higBA2
is a stress responsive locus, whose transcription changes in conditions encountered by
A. baumannii
in clinical environment and within the host. We show elevated expression of
higBA2
during stationary phase, under
iron deficiency
and downregulated expression after antibiotic (rifampicin) treatment.
...
PMID:The
higBA
Toxin-Antitoxin Module From the Opportunistic Pathogen
Acinetobacter baumannii
- Regulation, Activity, and Evolution. 2970 46