Project Title

Identification of Genetic Elements Involved in Alcaligenes faecalis' Inhibitory Mechanism Against Polymicrobial Species

Author Names

Abigail MathisFollow

Authors' Affiliations

Abigail Mathis,Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN

Location

Culp Room 217

Start Date

4-6-2022 10:00 AM

End Date

4-6-2022 10:15 AM

Faculty Sponsor’s Department

Health Sciences

Name of Project's Faculty Sponsor

Sean Fox

Additional Sponsors

Dr. Ranjan Chakraborty Dr. Erik Petersen

Classification of First Author

Undergraduate Student

Competition Type

Non-Competitive

Type

Boland Symposium

Project's Category

Microbiology

Abstract or Artist's Statement

The rise of antibiotic resistance of common human pathogens and the lack of development of novel therapeutic treatments has created a threat to global health. A unique source for potential novel treatments are from microorganisms, particularly within the complex, antagonistic polymicrobial interactions that take place in microbial communities. These unique mechanisms utilized by microorganisms to fight each other could potentially identify novel therapeutic targets for use at a clinical level, however, there is a lack of research in this area to determine its applicability. Alcaligenes faecalis is a Gram-negative bacterium that seldom causes human disease and has been observed in our lab to show competitive, contact-dependent inhibitory mechanisms against Bacillus species, Candida albicans, and Staphylococcus species. These bacterial and eukaryotic microbes are increasingly a common source of human disease and all exhibit increased incidences of drug resistance. In this study, genetic elements related to A. faecalis’ contact-dependent inhibitory mechanism were determined via transposon mutagenesis. Genomic sequencing was performed on mutant strains of A. faecalis that exhibited diminished inhibition or loss-of-function inhibition of the competing microbes. In A. faecalis mutant strains P2-9 and P1-42, the interrupted gene was identified as a FAD-binding oxidoreductase with a 94% and 90% match of nucleotide sequence. Mutant strain P2-25’s interrupted gene was identified as an MFS transporter with a 100% match and P2-30’s interrupted gene was identified as a mechanosensitive ion channel with a 100% match. Further analysis of these mutants is needed to determine their role in the mechanism of A. faecalis’ antimicrobial activity. The findings of this study may aid in the identification of new therapeutic targets for novel S. aureus, C. albicans, and Bacillus treatments.

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Apr 6th, 10:00 AM Apr 6th, 10:15 AM

Identification of Genetic Elements Involved in Alcaligenes faecalis' Inhibitory Mechanism Against Polymicrobial Species

Culp Room 217

The rise of antibiotic resistance of common human pathogens and the lack of development of novel therapeutic treatments has created a threat to global health. A unique source for potential novel treatments are from microorganisms, particularly within the complex, antagonistic polymicrobial interactions that take place in microbial communities. These unique mechanisms utilized by microorganisms to fight each other could potentially identify novel therapeutic targets for use at a clinical level, however, there is a lack of research in this area to determine its applicability. Alcaligenes faecalis is a Gram-negative bacterium that seldom causes human disease and has been observed in our lab to show competitive, contact-dependent inhibitory mechanisms against Bacillus species, Candida albicans, and Staphylococcus species. These bacterial and eukaryotic microbes are increasingly a common source of human disease and all exhibit increased incidences of drug resistance. In this study, genetic elements related to A. faecalis’ contact-dependent inhibitory mechanism were determined via transposon mutagenesis. Genomic sequencing was performed on mutant strains of A. faecalis that exhibited diminished inhibition or loss-of-function inhibition of the competing microbes. In A. faecalis mutant strains P2-9 and P1-42, the interrupted gene was identified as a FAD-binding oxidoreductase with a 94% and 90% match of nucleotide sequence. Mutant strain P2-25’s interrupted gene was identified as an MFS transporter with a 100% match and P2-30’s interrupted gene was identified as a mechanosensitive ion channel with a 100% match. Further analysis of these mutants is needed to determine their role in the mechanism of A. faecalis’ antimicrobial activity. The findings of this study may aid in the identification of new therapeutic targets for novel S. aureus, C. albicans, and Bacillus treatments.