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Potentiating antibiotic efficacy via perturbation of non-essential gene expression.

Otoupal, PB ; Eller, KA ; et al.
In: Communications biology, Jg. 4 (2021-11-05), Heft 1, S. 1267
academicJournal

Titel:
Potentiating antibiotic efficacy via perturbation of non-essential gene expression.
Autor/in / Beteiligte Person: Otoupal, PB ; Eller, KA ; Erickson, KE ; Campos, J ; Aunins, TR ; Chatterjee, A
Zeitschrift: Communications biology, Jg. 4 (2021-11-05), Heft 1, S. 1267
Veröffentlichung: London, United Kingdom : Nature Publishing Group UK, [2018]-, 2021
Medientyp: academicJournal
ISSN: 2399-3642 (electronic)
DOI: 10.1038/s42003-021-02783-x
Schlagwort:
  • Drug Resistance, Multiple, Bacterial
  • Escherichia coli drug effects
  • Klebsiella pneumoniae drug effects
  • Salmonella enterica drug effects
  • Anti-Bacterial Agents pharmacology
  • Escherichia coli genetics
  • Gene Expression drug effects
  • Klebsiella pneumoniae genetics
  • Salmonella enterica genetics
Sonstiges:
  • Nachgewiesen in: MEDLINE
  • Sprachen: English
  • Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • Language: English
  • [Commun Biol] 2021 Nov 05; Vol. 4 (1), pp. 1267. <i>Date of Electronic Publication: </i>2021 Nov 05.
  • MeSH Terms: Anti-Bacterial Agents / *pharmacology ; Escherichia coli / *genetics ; Gene Expression / *drug effects ; Klebsiella pneumoniae / *genetics ; Salmonella enterica / *genetics ; Drug Resistance, Multiple, Bacterial ; Escherichia coli / drug effects ; Klebsiella pneumoniae / drug effects ; Salmonella enterica / drug effects
  • References: United States Center for Disease Control and Prevention. Antibiotic Resistance Threats in the United States (Center for Disease Control and Prevention, 2019). ; Davies, S. C., Fowler, T., Watson, J., Livermore, D. M. & Walker, D. Infections and the rise of antimicrobial resistance. Lancet 381, 1606–1609 (2013). (PMID: 2348975610.1016/S0140-6736(13)60604-2) ; World Economic Forum. Global Risks 2014 Ninth Edition. https://reports.weforum.org/global-risks-2014/?doing_wp_cron=1630018056.6371810436248779296875 (2014). ; Tacconelli, E., Magrini, N., Kahlmeter, G. & Singh, N. Global priority list of antibiotic-resistant bacteria to guide research, discovery, and development of new antibiotics. World Health Organ. 27, 318–327 (2017). ; Review on Antimicrobial Resistance. Antimicrobial Resistance: Tackling a Crisis for the Health and Wealth of Nations (Review on Antimicrobial Resistance, 2014). ; Fernández, L., Breidenstein, E. B. M. & Hancock, R. E. W. Creeping baselines and adaptive resistance to antibiotics. Drug Resist. Update 14, 1–21 (2011). (PMID: 10.1016/j.drup.2011.01.001) ; Smith, P. A. & Romesberg, F. E. Combating bacteria and drug resistance by inhibiting mechanisms of persistence and adaptation. Nat. Chem. Biol. 3, 549–556 (2007). (PMID: 1771010110.1038/nchembio.2007.27) ; Courtney, C. M. et al. Photoexcited quantum dots for killing multidrug-resistant bacteria. Nat. Mater. 15, 529–534 (2016). (PMID: 2677988210.1038/nmat4542) ; Bikard, D. et al. Exploiting CRISPR-Cas nucleases to produce sequence-specific antimicrobials. Nat. Biotechnol. 32, 1146–1150 (2014). (PMID: 25282355431735210.1038/nbt.3043) ; Gomaa, A. A. et al. Programmable removal of bacterial strains by use of genome-targeting CRISPR/Cas systems. MBio. 5, e00928–13 (2014). (PMID: 24473129390327710.1128/mBio.00928-13) ; Otoupal, P. B., Erickson, K. E., Bordoy, A. E. & Chatterjee, A. CRISPR perturbation of gene expression alters bacterial fitness under stress and reveals underlying epistatic constraints. ACS Synth. Biol. 6, 94–107 (2017). (PMID: 2752943610.1021/acssynbio.6b00050) ; Nielsen, P. E. Peptide nucleic acid. A molecule with two identities. Acc. Chem. Res. 32, 624–630 (1999). (PMID: 10.1021/ar980010t) ; Courtney, C. M. & Chatterjee, A. Sequence-specific peptide nucleic acid-based antisense inhibitors of TEM-1 β-lactamase and mechanism of adaptive resistance. ACS Infect. Dis. 1, 253–263 (2015). (PMID: 2762274110.1021/acsinfecdis.5b00042) ; Nikravesh, A. et al. Antisense PNA accumulates in Escherichia coli and mediates a long post-antibiotic effect. Mol. Ther. 15, 1537–1542 (2007). (PMID: 1753426710.1038/sj.mt.6300209) ; Good, L., Awasthi, S. K., Dryselius, R., Larsson, O. & Nielsen, P. E. Bactericidal antisense effects of peptide-PNA conjugates. Nat. Biotechnol. 19, 360–364 (2001). (PMID: 1128359510.1038/86753) ; Bai, H. & Luo, X. A Search for Antibacterial Agents (ed. Bobbarala, V.) 319–344 (InTech, 2012). ; Eller, K. A. et al. Facile accelerated specific therapeutic (FAST) platform develops antisense therapies to counter multidrug-resistant bacteria. Commun. Biol. 4, 331 (2021). (PMID: 33712689795503110.1038/s42003-021-01856-1) ; Baba, T. et al. Construction of Escherichia coli K-12 in-frame, single-gene knockout mutants: the Keio collection. Mol. Syst. Biol. 2, 2006.0008 (2006). (PMID: 16738554168148210.1038/msb4100050) ; Erickson, K. E., Otoupal, P. B. & Chatterjee, A. Gene expression variability underlies adaptive resistance in phenotypically heterogeneous bacterial populations. ACS Infect. Dis. 1, 555–567 (2015). (PMID: 2762341010.1021/acsinfecdis.5b00095) ; Erickson, K. E., Otoupal, P. B. & Chatterjee, A. Transcriptome-level signatures in gene expression and gene expression variability during bacterial adaptive evolution. mSphere 2, 1–17 (2017). (PMID: 10.1128/mSphere.00009-17) ; Lee, S. et al. Targeting a bacterial stress response to enhance antibiotic action. Proc. Natl Acad. Sci. 106, 14570–14575 (2009). (PMID: 19706543273282710.1073/pnas.0903619106) ; Nichols, R. J. et al. Phenotypic landscape of a bacterial cell. Cell 144, 143–156 (2011). (PMID: 2118507210.1016/j.cell.2010.11.052) ; Chevereau, G. et al. Quantifying the determinants of evolutionary dynamics leading to drug resistance. PLoS Biol. 13, 1–18 (2015). (PMID: 10.1371/journal.pbio.1002299) ; Liu, A. et al. Antibiotic sensitivity profiles determined with an Escherichia coli gene knockout collection: generating an antibiotic bar code. Antimicrob. Agents Chemother. 54, 1393–1403 (2010). (PMID: 20065048284938410.1128/AAC.00906-09) ; Ayhan, D. H. et al. Sequence-specific targeting of bacterial resistance genes increases antibiotic efficacy. PLoS Biol. 14, 1–18 (2016). (PMID: 10.1371/journal.pbio.1002552) ; Ramos, J. L. et al. Mechanisms of solvent tolerance in gram-negative bacteria. Annu. Rev. Microbiol. 56, 743–768 (2002). (PMID: 1214249210.1146/annurev.micro.56.012302.161038) ; Du, D. et al. Structure of the AcrAB-TolC multidrug efflux pump. Nature 509, 512–515 (2014). (PMID: 24747401436190210.1038/nature13205) ; Pérez, A. et al. Involvement of the AcrAB-TolC efflux pump in the resistance, fitness, and virulence of Enterobacter cloacae. Antimicrob. Agents Chemother. 56, 2084–2090 (2012). (PMID: 22290971331835910.1128/AAC.05509-11) ; Pérez, A. et al. Cloning, nucleotide sequencing, and analysis of the AcrAB-TolC efflux pump of Enterobacter cloacae and determination of its involvement in antibiotic resistance in a clinical isolate. Antimicrob. Agents Chemother. 51, 3247–3253 (2007). (PMID: 17638702204321110.1128/AAC.00072-07) ; Duval, V. & Lister, I. M. MarA, SoxS and Rob of Escherichia coli—global regulators of multidrug resistance, virulence and stress response. Int. J. Biotechnol. Wellness Ind. 2, 101–124 (2013). (PMID: 248606364031692) ; McMurry, L. M., Oethinger, M. & Levy, S. B. Overexpression of marA, soxS, or acrAB produces resistance to triclosan in laboratory and clinical strains of Escherichia coli. FEMS Microbiol. Lett. 166, 305–309 (1998). (PMID: 977028810.1111/j.1574-6968.1998.tb13905.x) ; Alekshun, M. N. & Levy, S. B. The mar regulon: multiple resistance to antibiotics and other toxic chemicals. Trends Microbiol. 7, 410–413 (1999). (PMID: 1049894910.1016/S0966-842X(99)01589-9) ; Recacha, E. et al. Quinolone resistance reversion by targeting the SOS response. MBio. 8, 1–12 (2017). (PMID: 10.1128/mBio.00971-17) ; Cirz, R. T. et al. Complete and SOS-mediated response of Staphylococcus aureus to the antibiotic ciprofloxacin. J. Bacteriol. 189, 531–539 (2007). (PMID: 1708555510.1128/JB.01464-06) ; Miller, C. et al. SOS response induction by beta-lactams and bacterial defense against antibiotic lethality. Science 305, 1629–1631 (2004). (PMID: 1530876410.1126/science.1101630) ; Galhardo, R. S. et al. DinB upregulation is the sole role of the SOS response in stress-induced mutagenesis in Escherichia coli. Genetics 182, 55–68 (2009). (PMID: 19270270267484110.1534/genetics.109.100735) ; Kuban, W., Banach-Orlowska, M., Schaaper, R. M., Jonczyk, P. & Fijalkowska, I. J. Role of DNA polymerase IV in Escherichia coli SOS mutator activity. J. Bacteriol. 188, 7977–7980 (2006). (PMID: 16980447163630210.1128/JB.01088-06) ; Wagner, J. et al. The dinB gene encodes a novel E. coli DNA polymerase, DNA pol IV, involved in mutagenesis. Mol. Cell 4, 281–286 (1999). (PMID: 1048834410.1016/S1097-2765(00)80376-7) ; Tao, H. et al. Functional genomics: expression analysis of Escherichia coli growing on minimal and rich media. J. Bacteriol. 181, 6425–6440 (1999). (PMID: 1051593410377910.1128/JB.181.20.6425-6440.1999) ; Rutherford, B. J. et al. Functional genomic study of exogenous n-butanol stress in Escherichia coli. Appl. Environ. Microbiol. 76, 1935–1945 (2010). (PMID: 20118358283803010.1128/AEM.02323-09) ; Kaldalu, N., Mei, R. & Lewis, K. Killing by ampicillin and ofloxacin induces overlapping changes in Escherichia coli transcription profile. Antimicrob. Agents Chemother. 48, 890–896 (2004). (PMID: 1498278035307210.1128/AAC.48.3.890-896.2004) ; Reyes, L. H., Almario, M. P. & Kao, K. C. Genomic library screens for genes involved in n-butanol tolerance in Escherichia coli. PLoS ONE 6, e17678 (2011). (PMID: 21408113305090010.1371/journal.pone.0017678) ; Dwyer, D. J. et al. Antibiotics induce redox-related physiological alterations as part of their lethality. Proc. Natl Acad. Sci. 111, E2100–E2109 (2014). (PMID: 24803433403419110.1073/pnas.1401876111) ; Gutierrez, A. et al. β-Lactam antibiotics promote bacterial mutagenesis via an RpoS-mediated reduction in replication fidelity. Nat. Commun. 4, 1–9 (2013). (PMID: 10.1038/ncomms2607) ; Yeh, P., Tschumi, A. I. & Kishony, R. Functional classification of drugs by properties of their pairwise interactions. Nat. Genet. 38, 489–494 (2006). (PMID: 1655017210.1038/ng1755) ; Demidenko, E. & Miller, T. W. Statistical determination of synergy based on Bliss definition of drugs independence. PLoS ONE 14, e0224137 (2019). (PMID: 31765385687684210.1371/journal.pone.0224137) ; Otoupal, P. B., Cordell, W. T., Bachu, V., Sitton, M. J. & Chatterjee, A. Multiplexed deactivated CRISPR-Cas9 gene expression perturbations deter bacterial adaptation by inducing negative epistasis. Commun. Biol. 1, 1–13 (2018). (PMID: 10.1038/s42003-018-0135-2) ; Szklarczyk, D. et al. STRING v10: protein–protein interaction networks, integrated over the tree of life. Nucleic Acids Res. 43, D447–D452 (2015). (PMID: 2535255310.1093/nar/gku1003) ; Larson, M. H. et al. CRISPR interference (CRISPRi) for sequence-specific control of gene expression. Nat. Protoc. 8, 2180–2196 (2013). (PMID: 24136345392276510.1038/nprot.2013.132) ; Good, L., Awasthi, S. K., Dryselius, R., Larsson, O. & Nielsen, P. E. Bactericidal antisense effects of peptide–PNA conjugates. Nat. Biotechnol. 19, 360–364 (2001). (PMID: 1128359510.1038/86753) ; Keseler, I. M. et al. The EcoCyc database: reflecting new knowledge about Escherichia coli K-12. Nucleic Acids Res. 45, D543–D550 (2017). (PMID: 2789957310.1093/nar/gkw1003) ; Cui, L. et al. A CRISPRi screen in E. coli reveals sequence-specific toxicity of dCas9. Nat. Commun. 9, 1–10 (2018). (PMID: 10.1038/s41467-018-04209-5) ; Courtney, C. M. et al. Potentiating antibiotics in drug-resistant clinical isolates via stimuli-activated superoxide generation. Sci. Adv. 3, e1701776 (2017). (PMID: 28983513562798310.1126/sciadv.1701776) ; Erickson, K. E., Madinger, N. E. & Chatterjee, A. Draft genome sequences of clinical isolates of multidrug-resistant Acinetobacter baumannii. Genome Announc. 5, e01547–16 (2017). (PMID: 28153899528968510.1128/genomeA.01547-16) ; Erickson, K. E., Madinger, N. E. & Chatterjee, A. Draft genome sequence for a clinical isolate of vancomycin-resistant Enterococcus faecalis. Genome Announc. 4, e00584–16 (2016). (PMID: 27340066491940510.1128/genomeA.00584-16) ; Aunins, T. R., Erickson, K. E. & Chatterjee, A. Transcriptome-based design of antisense inhibitors potentiates carbapenem efficacy in CRE Escherichia coli. Proc. Natl Acad. Sci. 117, 30699–30709 (2020). (PMID: 33199638772019610.1073/pnas.1922187117) ; Sturge, C. R. et al. AcrAB-TolC inhibition by peptide-conjugated phosphorodiamidate morpholino oligomers restores antibiotic activity in vitro and in vivo. ACS Infect. Dis. 5, 1446–1455 (2019). (PMID: 3111993510.1021/acsinfecdis.9b00123) ; Tamae, C. et al. Determination of antibiotic hypersensitivity among 4000 single-gene-knockout mutants of Escherichia coli. J. Bacteriol. 190, 5981–5988 (2008). (PMID: 18621901251952510.1128/JB.01982-07) ; Weiss, S. J., Mansell, T. J., Mortazavi, P., Knight, R. & Gill, R. T. Parallel mapping of antibiotic resistance alleles in Escherichia coli. PLoS ONE 11, 1–18 (2016). (PMID: 10.1371/journal.pone.0146916) ; Baym, M., Stone, L. K. & Kishony, R. Multidrug evolutionary strategies to reverse antibiotic resistance. Science 351, aad3292 (2016). (PMID: 26722002549698110.1126/science.aad3292) ; Hegreness, M., Shoresh, N., Damian, D., Hartl, D. & Kishony, R. Accelerated evolution of resistance in multidrug environments. Proc. Natl Acad. Sci. 105, 13977–13981 (2008). (PMID: 18779569254456410.1073/pnas.0805965105) ; Cottarel, G. & Wierzbowski, J. Combination drugs, an emerging option for antibacterial therapy. Trends Biotechnol. 25, 547–555 (2007). (PMID: 1799717910.1016/j.tibtech.2007.09.004) ; Cirz, R. T. et al. Inhibition of mutation and combating the evolution of antibiotic resistance. PLoS Biol. 3, 1024–1033 (2005). (PMID: 10.1371/journal.pbio.0030176) ; Nevozhay, D., Adams, R. M., van Itallie, E., Bennett, M. R. & Balázsi, G. Mapping the environmental fitness landscape of a synthetic gene circuit. PLoS Comput. Biol. 8, e1002480 (2012). (PMID: 22511863332517110.1371/journal.pcbi.1002480) ; Trindade, S. et al. Positive epistasis drives the acquisition of multidrug resistance. PLoS Genet. 5, e1000578 (2009). (PMID: 19629166270697310.1371/journal.pgen.1000578) ; Romero, P. A. & Arnold, F. H. Exploring protein fitness landscapes by directed evolution. Nat. Rev. Mol. Cell Biol. 10, 866–876 (2009). (PMID: 19935669299761810.1038/nrm2805) ; Lenski, R. E., Rose, M. R., Simpson, S. C. & Tadler, S. C. Long-term experimental evolution in Escherichia coli. Adaptation and divergence during 2000 generations. Am. Nat. 138, 1315–1341 (1991). (PMID: 10.1086/285289) ; Langmead, B. & Salzberg, S. L. Fast gapped-read alignment with Bowtie 2. Nat. Methods 9, 357–359 (2012). (PMID: 22388286332238110.1038/nmeth.1923) ; Quinlan, A. R. & Hall, I. M. BEDTools: a flexible suite of utilities for comparing genomic features. Bioinformatics 26, 841–842 (2010). (PMID: 20110278283282410.1093/bioinformatics/btq033) ; Taunins. taunins/pna_finder: First release of PNA Finder. https://doi.org/10.5281/ZENODO.4426813 (2021). ; Li, H. et al. The Sequence Alignment/Map format and SAMtools. Bioinformatics 25, 2078–2079 (2009). (PMID: 19505943272300210.1093/bioinformatics/btp352)
  • Grant Information: DGE1144083 National Science Foundation (NSF); MCB1714564 National Science Foundation (NSF); D17AP00024 United States Department of Defense | Defense Advanced Research Projects Agency (DARPA)
  • Substance Nomenclature: 0 (Anti-Bacterial Agents)
  • Entry Date(s): Date Created: 20211106 Date Completed: 20211217 Latest Revision: 20230209
  • Update Code: 20231215
  • PubMed Central ID: PMC8571399

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