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Research description
The effects of increasing atmospheric CO2 concentrations include mild rises in sea level and uncontrolled global warming. To lower existing levels of atmospheric CO2, we must access untapped renewable resources, such as solar power. To become competitive with wind and hydro-power, solar energy requires an efficient means of energy storage.
Energy storage in carbon-to-carbon bonds represents an energy dense means of storage that can be integrated into existing infrastructure. It can be achieved through photosynthesis or electrosynthesis. Electrosynthesis produces organic compounds via the same net reaction as photosynthesis: carbon dioxide and water are converted to organic compounds and oxygen. However, the energy source for electrosynthesis is electricity, which may ultimately come from sunlight through photovoltaics. Electrosynthesis is more efficient than photosynthesis because energy flow is primarily diverted to product rather than excess biomass. Microbial electrosynthesis (ME) offers myriad advantages over abiotic catalysts, including decreased toxicity and cost, as well as the ability to produce specific products at high efficiency. Although ME traditionally was researched as a means to produce hydrogen, it also presents a path toward fossil-fuel independent organic compound production. Acetogens represent potentially attractive catalysts for ME because they already contain the Wood-Ljungdhal pathway for carbon dioxide reduction, allowing for carbon dioxide sequestration into organic compounds. Many acetogens also have genetic systems available and exhibit a diversity of metabolisms. Moreover, acetogens have recently been shown to be capable of ME from a graphite electrode. However, it is currently unknown how acetogens are capable of converting electrons and carbon dioxide into organic compounds. In order to determine what physiological components are key to an efficient means to store solar energy in organic compounds, we seek to examine the system preference, metabolic activity, and gene expression of acetogens in a ME system.
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