The profiling revealed that fusaricidins strongly activated SigA, a protein that regulates RNA polymerase to control cell growth. Kinetic analyses of transcriptional responses showed that differentially regulated genes represent several metabolic pathways, including those regulating proline levels, ion transport, amino acid transport, and nucleotide metabolism. However, when the Fe concentration was gradually reduced, PerR activity in response to peroxide was restored. In B. subtilis, iron is transported through 3 steps: threonine, glycine, and 2,3-dihydroxybenzoate are used as precursors to synthesize bacillibactin by dhbCAEBF; BB is then exported from the cell by YmfE to combine with iron; and Fe-BB is shuttled back into the cell via the ABC-type transporter FeuABC-YusV. To achieve intracellular iron release, Fe-BB is then hydrolyzed by the Fe-BB esterase BesA and iron is used by the cell. The process of iron transport is controlled by 3 regulatory proteins: Fur, Mta, and Btr. When iron concentration is low, derepression of Fur leads to increased activity of Mta and Btr, which accelerates BB outflow and Fe-BB uptake. In this manner, all the genes related to iron transport are upregulated upon fusaricidin treatment of B. subtilis, robustly stimulating iron transport. We next compared our data with the results from other studies. Cluster analysis was used to determine whether other antibiotic treatments had a similar profile to that of fusaricidin. NO, vancomycin, bacitracin, iron starvation, Fe limitation, and daptomycin were all used in the comparison. As shown in Figure 8, the data from the Fe limitation treatment had the highest similarity to those from our experiment. This suggests that iron is an essential component for bacteria to resist treatment with toxins. Forty additional antibiotics were also chosen to compare with the fusaricidin treatment in this study. This comparison revealed that the treatment of B. subtilis with fusaricidin elicited a profile most similar with that of triclosan. Fusaricidin addition could lead B. subtilis’s XL-184 membrane to be destroyed and more OH produced which affected the biosynthesis of protein and nucleic acid in the cells at the initial phase. However, B. subtilis could recover its growth in the late phase because of the congeries of the cells in the culture. It is suggested that the novel antibactin should stimulate the cells to secrete more and more OH to disturb the growth and prevent the cells to congest simultaneously. The transcriptome analyses indicate that fusaricidin induced sets of genes shown previously to be induced by exposure to membrane-active compounds. The TCS was significantly induced by fusaricidin, and genetic studies indicated that SigA was sensitive to this change. These results were consistent with the notion that this type of antibiotic acts primarily on the cell membrane. Apparently, B. subtilis is one of microorganisms which is able to alter its gene expression pattern in response to fusaricidin to develop resistance to antibiotic treatment and some other environmental changing. G protein-coupled receptors are one of the pharmaceutically most important protein families, and the targets of around one third of present day drugs. They mediate the transmission of signals from the exterior to the interior of a cell by binding signaling agents and, via conformational changes, eliciting intracellular responses. GPCRs consist of seven membranecrossing helices. The binding pockets of the native small molecule ligands, i.e. orthosteric binding sites, are situated in the middle of the helical bundle in the Class A GPCR structures that have been determined so far. There are still many GPCR targets for which no structure or ligands are known.