ABC superfamily transporter Rv1273c of Mycobacterium tuberculosis acts as a multidrug efflux pump.
Mycobacterium tuberculosis
ABC transporter
antibiotic resistance
biofilm formation
efflux pump
multidrug efflux
Journal
FEMS microbiology letters
ISSN: 1574-6968
Titre abrégé: FEMS Microbiol Lett
Pays: England
ID NLM: 7705721
Informations de publication
Date de publication:
17 01 2023
17 01 2023
Historique:
received:
20
05
2023
revised:
17
10
2023
accepted:
24
10
2023
medline:
15
11
2023
pubmed:
26
10
2023
entrez:
26
10
2023
Statut:
ppublish
Résumé
Efflux pump-mediated drug resistance in bacteria is a common occurrence effective for the general survival of the organism. The Mycobacterium tuberculosis genome has an abundance of adenosine triphosphate (ATP) dependent cassette transporter genes but only a handful of them are documented for their contribution to drug resistance. In this study, we inspected the potential of an ABC transporter Rv1273c from M. tuberculosis as a multidrug efflux pump and a contributor to intrinsic drug resistance. Expression of Rv1273c in Escherichia coli and M. smegmatis conferred tolerance to various structurally unrelated antibiotics. Lower accumulation of fluoroquinolones in intact E. coli and M. smegmatis cells expressing the transporter implied its active efflux activity. Energy-dependent efflux by Rv1273c was observed in real time using the lipophilic dye Nile Red. Expression of Rv1273c also resulted in an increase in biofilm formation by E. coli and M. smegmatis cells. Overall, the results indicate the possibility that Rv1273c might be a multidrug transporter with a wide substrate range and a probable contributor to biofilm formation.
Identifiants
pubmed: 37881010
pii: 7330199
doi: 10.1093/femsle/fnad114
pii:
doi:
Substances chimiques
ATP-Binding Cassette Transporters
0
Membrane Transport Proteins
0
Anti-Bacterial Agents
0
Bacterial Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of FEMS.