Elucidating the Genetic Basis of Hydrogen Sulfide Production in Desulfovibrio piger

Faculty Mentor

Andrea Castillo

Presentation Type

Poster

Start Date

5-8-2024 9:00 AM

End Date

5-8-2024 10:45 AM

Location

PUB NCR

Primary Discipline of Presentation

Biology

Abstract

The metabolic byproducts of organisms within the human gut microbiome can have both beneficial and deleterious effects on human health. Sulfur-reducing bacteria make up a significant amount of the gut microbiota, and of these organisms, Desulfovibrio piger is the most abundant. D. piger reduces exogenous sources of sulfur to form its primary metabolite, hydrogen sulfide (H2S), which is implicated in a range of diseases due to its pro-inflammatory and cytotoxic capabilities within the human body. Overgrowth of D. piger has been strongly correlated to multiple sclerosis, Chron’s disease, and several other inflammatory diseases, through fecal studies which compare the microbiota composition of healthy and diseased individuals, suggesting a link between high levels of H2S and disease severity. However, there exists little information on the genetic foundation of H2S production in D. piger. I aim to determine which genes are required for sulfur reduction in this organism to provide insights into potential therapeutic targets for these diseases. Through sequential cloning, putative H2S producing genes from D. piger will be introduced into the model organism, Escherichia coli, and the resulting mutants will be screened for H2S production to determine which genes are essential for sulfur reduction. Selected genes include those that code for the dissimilatory sulfite reductase enzyme, as well as genes that code for prerequisite enzymes in the sulfur reduction process. If the presence of these genes confers H2S production in E. coli, a more concrete understanding of the genetic control of this metabolic process can be inferred.

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May 8th, 9:00 AM May 8th, 10:45 AM

Elucidating the Genetic Basis of Hydrogen Sulfide Production in Desulfovibrio piger

PUB NCR

The metabolic byproducts of organisms within the human gut microbiome can have both beneficial and deleterious effects on human health. Sulfur-reducing bacteria make up a significant amount of the gut microbiota, and of these organisms, Desulfovibrio piger is the most abundant. D. piger reduces exogenous sources of sulfur to form its primary metabolite, hydrogen sulfide (H2S), which is implicated in a range of diseases due to its pro-inflammatory and cytotoxic capabilities within the human body. Overgrowth of D. piger has been strongly correlated to multiple sclerosis, Chron’s disease, and several other inflammatory diseases, through fecal studies which compare the microbiota composition of healthy and diseased individuals, suggesting a link between high levels of H2S and disease severity. However, there exists little information on the genetic foundation of H2S production in D. piger. I aim to determine which genes are required for sulfur reduction in this organism to provide insights into potential therapeutic targets for these diseases. Through sequential cloning, putative H2S producing genes from D. piger will be introduced into the model organism, Escherichia coli, and the resulting mutants will be screened for H2S production to determine which genes are essential for sulfur reduction. Selected genes include those that code for the dissimilatory sulfite reductase enzyme, as well as genes that code for prerequisite enzymes in the sulfur reduction process. If the presence of these genes confers H2S production in E. coli, a more concrete understanding of the genetic control of this metabolic process can be inferred.