Detection of 2,4,6-trinitrotoluene (TNT) has been extensively studied since it is a common explosive filling for landmines, posing significant threats to the environment and human safety. The rapid advances in synthetic biology give new hope to detect such toxic and hazardous compounds in a more sensitive and safe way. Biosensor construction anticipates finding sensing elements able to detect TNT. As TNT can induce some physiological responses in E. coli, it may be useful to define the sensing elements from E. coli to detect TNT. An E. coli MG1655 genomic promoter library containing nearly 5,400 elements was constructed. Five elements, yadG, yqgC, aspC, recE, and topA, displayed high sensing specificity to TNT and its indicator compounds 1,3-DNB and 2,4-DNT. Based on this, a whole cell biosensor was constructed using E. coli, in which green fluorescent protein was positioned downstream of the five sensing elements via genetic fusion. The threshold value, detection time, EC200 value, and other aspects of five sensing elements were determined and the minimum responding concentration to TNT was 4.75 mg/L. According to the synthetic biology, the five sensing elements enriched the reservoir of TNT-sensing elements, and provided a more applicable toolkit to be applied in genetic routes and live systems of biosensors in future.

p43 is a cofactor of aminoacyl-tRNA synthetase in mammals that effectively inhibits angiogenesis. However, the role of p43 in angiogenesis remains unclear. In the present study, we examined the effects of p43 on angiogenesis using human microvascular endothelial cells-1 (HMEC-1) cells as a model. Our microarray data showed that p43 regulated a number of cytokines, and the majoity of these are involved in the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway. IP-10 was previously shown to inhibit angiogenesis and suppress tumor growth via the JAK-STAT signaling pathway in vitro and in vivo. Our results showed that p43 induces both the mRNA and protein expression of IP-10. Furthermore, we demonstrated that p43 exerted an effect on the JAK-STAT signaling pathway by regulating key factors of the pathway. Using a JAK inhibitor, AG490, we studied the effect of p43 on HMEC-1 cells by blocking the JAK-STAT pathway. We found that AG490 inhibited the induction of IP-10 expression by p43, and suppressed the inhibitory effect of p43 on tubule formation and cell migration in HMEC-1 cells. We concluded that p43 inhibits tubule formation and cell migration by inducing IP-10 through the JAK-STAT signaling pathway, and blocking the JAK-STAT pathway with AG490 diminishes the inhibitory effects of p43 on angiogenesis.