The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>

<i>Acinetobacter baumannii</i> is an opportunistic human pathogen responsible for numerous severe nosocomial infections. Genome analysis on the <i>A. baumannii</i> clinical isolate 04117201 revealed the presence of 13 two-component signal transduction systems (TCS). Of these,...

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Main Authors: Sarah K. Giles, Uwe H. Stroeher, Bhavya Papudeshi, Robert A. Edwards, Jessica AP. Carlson-Jones, Michael Roach, Melissa H. Brown
Format: Article
Language:English
Published: MDPI AG 2022-05-01
Series:Microorganisms
Subjects:
Online Access:https://www.mdpi.com/2076-2607/10/5/985
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author Sarah K. Giles
Uwe H. Stroeher
Bhavya Papudeshi
Robert A. Edwards
Jessica AP. Carlson-Jones
Michael Roach
Melissa H. Brown
author_facet Sarah K. Giles
Uwe H. Stroeher
Bhavya Papudeshi
Robert A. Edwards
Jessica AP. Carlson-Jones
Michael Roach
Melissa H. Brown
author_sort Sarah K. Giles
collection DOAJ
description <i>Acinetobacter baumannii</i> is an opportunistic human pathogen responsible for numerous severe nosocomial infections. Genome analysis on the <i>A. baumannii</i> clinical isolate 04117201 revealed the presence of 13 two-component signal transduction systems (TCS). Of these, we examined the putative TCS named here as StkSR. The <i>stkR</i> response regulator was deleted via homologous recombination and its progeny, Δ<i>stkR</i>, was phenotypically characterized. Antibiogram analyses of Δ<i>stkR</i> cells revealed a two-fold increase in resistance to the clinically relevant polymyxins, colistin and polymyxin B, compared to wildtype. PAGE-separation of silver stained purified lipooligosaccharide isolated from Δ<i>stkR</i> and wildtype cells ruled out the complete loss of lipooligosaccharide as the mechanism of colistin resistance identified for Δ<i>stkR</i>. Hydrophobicity analysis identified a phenotypical change of the bacterial cells when exposed to colistin. Transcriptional profiling revealed a significant up-regulation of the <i>pmrCAB</i> operon in Δ<i>stkR</i> compared to the parent, associating these two TCS and colistin resistance. These results reveal that there are multiple levels of regulation affecting colistin resistance; the suggested ‘cross-talk’ between the StkSR and PmrAB two-component systems highlights the complexity of these systems.
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spelling doaj.art-5e5fac6182364de28b497785bc4a502d2023-11-23T12:16:02ZengMDPI AGMicroorganisms2076-26072022-05-0110598510.3390/microorganisms10050985The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>Sarah K. Giles0Uwe H. Stroeher1Bhavya Papudeshi2Robert A. Edwards3Jessica AP. Carlson-Jones4Michael Roach5Melissa H. Brown6College of Science and Engineering, Flinders University, Adelaide, SA 5042, AustraliaCollege of Science and Engineering, Flinders University, Adelaide, SA 5042, AustraliaCollege of Science and Engineering, Flinders University, Adelaide, SA 5042, AustraliaCollege of Science and Engineering, Flinders University, Adelaide, SA 5042, AustraliaCollege of Science and Engineering, Flinders University, Adelaide, SA 5042, AustraliaCollege of Science and Engineering, Flinders University, Adelaide, SA 5042, AustraliaCollege of Science and Engineering, Flinders University, Adelaide, SA 5042, Australia<i>Acinetobacter baumannii</i> is an opportunistic human pathogen responsible for numerous severe nosocomial infections. Genome analysis on the <i>A. baumannii</i> clinical isolate 04117201 revealed the presence of 13 two-component signal transduction systems (TCS). Of these, we examined the putative TCS named here as StkSR. The <i>stkR</i> response regulator was deleted via homologous recombination and its progeny, Δ<i>stkR</i>, was phenotypically characterized. Antibiogram analyses of Δ<i>stkR</i> cells revealed a two-fold increase in resistance to the clinically relevant polymyxins, colistin and polymyxin B, compared to wildtype. PAGE-separation of silver stained purified lipooligosaccharide isolated from Δ<i>stkR</i> and wildtype cells ruled out the complete loss of lipooligosaccharide as the mechanism of colistin resistance identified for Δ<i>stkR</i>. Hydrophobicity analysis identified a phenotypical change of the bacterial cells when exposed to colistin. Transcriptional profiling revealed a significant up-regulation of the <i>pmrCAB</i> operon in Δ<i>stkR</i> compared to the parent, associating these two TCS and colistin resistance. These results reveal that there are multiple levels of regulation affecting colistin resistance; the suggested ‘cross-talk’ between the StkSR and PmrAB two-component systems highlights the complexity of these systems.https://www.mdpi.com/2076-2607/10/5/985<i>pmrCAB</i>hydrophobicitylipid AadherencephosphoethanolamineTCS
spellingShingle Sarah K. Giles
Uwe H. Stroeher
Bhavya Papudeshi
Robert A. Edwards
Jessica AP. Carlson-Jones
Michael Roach
Melissa H. Brown
The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>
Microorganisms
<i>pmrCAB</i>
hydrophobicity
lipid A
adherence
phosphoethanolamine
TCS
title The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>
title_full The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>
title_fullStr The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>
title_full_unstemmed The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>
title_short The StkSR Two-Component System Influences Colistin Resistance in <i>Acinetobacter baumannii</i>
title_sort stksr two component system influences colistin resistance in i acinetobacter baumannii i
topic <i>pmrCAB</i>
hydrophobicity
lipid A
adherence
phosphoethanolamine
TCS
url https://www.mdpi.com/2076-2607/10/5/985
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