The World Health Organization has reported Pseudomonas aeruginosa as the second most critical pathogen because of its antibiotic resistance. Once infected, the host immune response sends macrophages to phagocytize the foreign bodies. Once digested, macrophages commence defense strategies to kill the bacteria. This is achieved by increasing copper levels as toxic anti-microbial effector in the phagosomes. Normally high levels of copper and other metals will kill bacteria, but P. aeruginosa has a highly effective copper homeostasis system. A complex network of copper sensors, regulators and chaperones work in tandem to control the levels of copper in the different cell compartments. Certain periplasmic proteins are upregulated in the presence of high copper levels and assist in maintaining copper homeostasis. Studies have showed a difference in phenotypes of mutant cells lacking periplasmic proteins when compared to the wild strains in response to increasing copper levels. Complementing the mutant strains with a vector construct containing the missing gene is necessary to validate the results from previous studies. This study isolated the periplasmic genes PA2807 and PtrA and inserted them into the pHERD 30T vector to transform competent cells that could then be used to complement P. aeruginosa mutant strains.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Kloeckner, Allison

Publisher

• Worcester Polytechnic Institute

Identifier

• 20901
• E-project-043021-123441

Advisor

• Argüello, José M.

Year

• 2021

Date created

• 2021-04-30

Resource type

• Major Qualifying Project

Major

• Biochemistry

Rights statement

• In Copyright