Title: The Effect of Acetone and Nitric Oxide on the expression of genes fadA, scoA, and scoB and potential regulation via the CrdRS two component system in Heliobacter Pylori
Department: Biology
Description: Heliobacter pylori is a bacterium present in almost half of the human population, and is a cause of stomach ulcers and gastric cancer. We hypothesize that its co-evolution with humans allowed H. pylori to evolve the ability to metabolize acetone. Acetone is a ketone body present at higher concentrations during malnourishment, and acetyl-CoA generated from acetone is a key molecule for H. pylori. The full metabolic pathway of acetone use is encoded by the operons acxABC and fadA/scoAB, the focus of my project. scoA and scoB encode enzymes involved in the metabolism of acetoacetate into acetoacetyl-CoA via succinyl-CoA. FadA facilitates the transfer of acetoacetyl-CoA into 2 acetyl-CoA via CoA. My project aims to investigate how mRNA expression of fadA, scoA, and scoB is impacted by the presence of acetone and nitric oxide. The Two Component System, CrdRS, controls expression of acxABC, thus we hypothesize it controls fadA/scoAB as well.
Hometown: Huntsville, Alabama
Advisor: Mark Forsyth
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