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