A Fragrance-Producing Carbon Monoxide Detector

Carbon monoxide (CO) is a toxic colorless and odorless gas that results in thousands of fatalities a year, yet most detectors are based upon sight and sound that exclude the blind and the deaf. Furthermore, current sensors rely upon upon the presence of electricity and power, and are thus unable to act in scenarios of natural disasters when CO leaks are most likely.

This project introduces a CO-sensing mechanism into E.coli using a CooA transcription activator and corresponding pCooF promoter to regulate the expression of a methyl salicylate pathway (pchBA and BSMT genes). The pathway converts the endogenous molecule chorismate into salicylic acid and then methyl salicylate, producing a wintergreen smell in the presence of CO. This CO sensor has implications for not only the disabled, but also commercial use in cases of natural disaster due to its cost efficiency and transportability.

General Overview

Pathway Overview

The pchA protein (isochorismate synthase) converts chorismate to isochorismate. The pchB protein (isochorismate pyruvate-lyase) then converts isochorismate to salicylic acid. Finally, the BSMT protein (SAM benzoic acid/salicylic acid carboxyl methyltransferase I) converts salicylic acid to methyl salicylate, the desired wintergreen smell.

Plasmid

Why?

Carbon monoxide (CO) is a toxic gas that is odorless, colorless, and initially nonirritating, which further exacerbates the harmful effects of CO. It is a product of partial or incomplete combustion of organic matter in an oxygen-deprived environment, hindering in the complete oxidation of carbon dioxide. It emanates from anything that produces combustion fumes and is widely present in domestic or industrial settings (e.g. car engines, fuel-burning space heater, gas heaters, fireplaces, furnace, cooking equipment, etc.).

Inhaling CO can lead to hypoxic injury, severe nervous system damage, brain lipid peroxidation, and death. CO can bind to myoglobin, hemoglobin, and mitochondrial cytochrome oxidase, all three of which are vital to the proper utilization of oxygen in our bodies. The presence of CO in our system can drastically hinder the oxygen-carrying capacity of blood and inhibit the delivery and proper transport of oxygen by the blood.

Community Coverage

Check out some articles about us and our CO project online!

KUT: http://txst.us/1I7jW9R

KXAN: http://kxan.com/2015/07/29/lasa-students-developing-bacteria-to-improve-carbon-monoxide-detectors/

Works Cited

Foresti, Roberta, Jehad Hammad, James E. Clark, Tony R. Johnson, Brian E. Mann, Andreas Friebe, Colin J. Green, and Roberto Motterlini. Vasoactive Properties of CORM-3. British Journal of Pharmacology. Nature Publishing Group, 2004. Web. 18 Sept. 2015.

He, Yiping, Tamas Gaal, Russell Karls, Timothy J. Donohue, Richard L. Gourse, and Gary P. Roberts. Transcription and Activation by CooA, the CO-sensing Molecule from Rhodospirillum Rhubrum. The Journal of Biological Chemistry. The American Society of Biochemistry and Molecular Biology, 1999. Web. 17 Sept. 2015. .

Youn, Hwan, Robert L. Kerby, Mary Conard, and Gary P. Roberts. Functionally Critical Elements of CooA-Related CO Sensors. US National Library of Medicine. American Society of Microbiology, 2004. Web. 18 Sept. 2015.