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Evolution of Copper Resistance in Es...

Boyd, Sada Michelle.

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Evolution of Copper Resistance in Escherichia coli.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Evolution of Copper Resistance in Escherichia coli./
作者:	Boyd, Sada Michelle.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2020,
面頁冊數:	92 p.
附註:	Source: Dissertations Abstracts International, Volume: 81-12, Section: B.
Contained By:	Dissertations Abstracts International81-12B.
標題:	Biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=27832333
ISBN:	9798645471002

Evolution of Copper Resistance in Escherichia coli.
Boyd, Sada Michelle.

Evolution of Copper Resistance in Escherichia coli. - Ann Arbor : ProQuest Dissertations & Theses, 2020 - 92 p.

Source: Dissertations Abstracts International, Volume: 81-12, Section: B.

Thesis (Ph.D.)--North Carolina Agricultural and Technical State University, 2020.

This item must not be sold to any third party vendors.

Multi-drug resistant (MDR) bacteria are a growing worldwide public health concern. Metals such as copper, iron, and silver have been used as antimicrobial agents for many years due to their effectiveness in limiting the growth of a broad range of microorganisms. The use of metals as antimicrobials has generated renewed interest due to the rise of antibiotic resistant strains worldwide. Particular attention has been given to the antimicrobial use of copper (Cu), due to its unique and effective killing ability. However, little attention has been given to the ability of bacteria to evolve resistance to copper. Here, experimental evolution along with whole-genome and RNA-sequencing was used to investigate the potential genomic mechanisms involved in the evolution of Cu2+ resistance in Escherichia coli K-12 MG1655. In addition, whether adaptions to Cu2+-resistance lead to correlated resistances in the presence of other metals and antibiotics were also assessed. Results have generally indicated that Cu2+ resistance occurs rapidly in E. coli (37 days) via de novo mutations and gene expression changes. The whole-genome sequencing data suggests that the evolution of Cu2+ resistance occurs due to mutations in the cpxA gene, specifically within the HAMP domain likely leading to constitutive activation. RNAseq data showed the upregulation of genes mediated by ATP-Binding Cassettes (ABC) transporters and downregulation of genes involved in bacteria flagella structural components/synthesis may be of particular importance for Cu2+ resistance. It was also determined that mutations associated with Cu2+ resistant cause evolutionary trade-offs for resistance to other antimicrobials: iron, gallium, copper oxide nanoparticles, bacitracin, sulfonamide and chloramphenicol. In conclusion, these analyses indicate that specific mutations in cpxA and certain gene expression changes may play a role in Cu2+ resistance. Furthermore, adaptations to excess Cu2+ limits E. coli ability to grow in the presence of other antimicrobials.

ISBN: 9798645471002Subjects--Topical Terms:

522710
Biology.
Subjects--Index Terms:

Copper

Evolution of Copper Resistance in Escherichia coli.
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520 $a Multi-drug resistant (MDR) bacteria are a growing worldwide public health concern. Metals such as copper, iron, and silver have been used as antimicrobial agents for many years due to their effectiveness in limiting the growth of a broad range of microorganisms. The use of metals as antimicrobials has generated renewed interest due to the rise of antibiotic resistant strains worldwide. Particular attention has been given to the antimicrobial use of copper (Cu), due to its unique and effective killing ability. However, little attention has been given to the ability of bacteria to evolve resistance to copper. Here, experimental evolution along with whole-genome and RNA-sequencing was used to investigate the potential genomic mechanisms involved in the evolution of Cu2+ resistance in Escherichia coli K-12 MG1655. In addition, whether adaptions to Cu2+-resistance lead to correlated resistances in the presence of other metals and antibiotics were also assessed. Results have generally indicated that Cu2+ resistance occurs rapidly in E. coli (37 days) via de novo mutations and gene expression changes. The whole-genome sequencing data suggests that the evolution of Cu2+ resistance occurs due to mutations in the cpxA gene, specifically within the HAMP domain likely leading to constitutive activation. RNAseq data showed the upregulation of genes mediated by ATP-Binding Cassettes (ABC) transporters and downregulation of genes involved in bacteria flagella structural components/synthesis may be of particular importance for Cu2+ resistance. It was also determined that mutations associated with Cu2+ resistant cause evolutionary trade-offs for resistance to other antimicrobials: iron, gallium, copper oxide nanoparticles, bacitracin, sulfonamide and chloramphenicol. In conclusion, these analyses indicate that specific mutations in cpxA and certain gene expression changes may play a role in Cu2+ resistance. Furthermore, adaptations to excess Cu2+ limits E. coli ability to grow in the presence of other antimicrobials.
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