Data from: The diversity of cellular systems involved in carbonate precipitation by Escherichia coli

Climate change is increasing the need to limit levels of anthropogenic CO2
released into the atmosphere. One approach being investigated is to
generate products based on microbially induced carbonate precipitation
(MICP), which can trap CO2 as CaCO3. We recently identified a novel MICP
pathway in bacteria that is initiated by Ca2+ toxicity in cells, causing
extracellular CO2 to be trapped as CO32- by Escherichia coli, although the
yield of precipitated CaCO3 remained low (in the milligram range). In this
work, we used the E. coli Keio gene knock-out library to identify 54 genes
involved in MICP in E. coli, which could be broadly characterized into
four groups: central metabolism, iron metabolism, cell architecture, and
transport. The role of central metabolism appears to be crucial in
maintaining alkaline conditions surrounding the cell that promote CaCO3
precipitation. The role of iron metabolism was less clear, although the
results suggest that growth rate influences the initiation of MICP. While
the impact of repeating polymeric structures on cell surfaces promoting
MICP is well established, our results suggest that other structural
features may play a role, including fimbriae and flagella. Finally, the
results confirmed that Ca2+ transport is central to MICP under calcium
stress. The results further suggest that the ZntB efflux pump may play a
previously unidentified role in Ca2+ transport in E. coli. By
overexpressing some of these genes, our work suggests that there are
several previously unidentified cellular mechanisms that could serve as a
target for enhanced MICP in E. coli. By incorporating these processes into
MICP pathways in E. coli, it may be possible to increase the volume of CO2
fixed using this pathway and yield potentially new products that can
replace CO2 intensive products, such as precipitated calcium carbonates
(PCCs) for industry.