Since BCAID comes from a multi-system design, the parts we've built to support the project are quite diverse, extraordinary and novel. Our parts are mainly concentrated in the healing promoting module, the blue light-activated cellulose degradation module and the red light-activated suicide module. We carefully submitted all the components we developed to perform one particular function into Basic Parts in Registry, then each basic part is combined with others orderly and meaningfully to compose functional Composite Parts, and finally submitted in Registry.

The red/far-red light suicide control system REDMAP is so sensitive to light that as low as 0.1 mW∙cm-2 red light (far-red light) can be sensed. The specific mechanism of this system is that when exposed to red light (660 nm), the transactivator (FHY1–VP64) can specifically bind to the light sensor domain (ΔPhyA–Gal4) in the presence of the photosensitive pigment PCB. Then, the complex protein translocates into the nucleus where it can bind to its synthetic promoter (P5×UAS, 5×UAS-P(hCMVmin)) to initiate expression of MazF. Following exposure to far-red light (730 nm), the transactivator dissociates from the light sensor domain (ΔPhyA–Gal4), thereby terminating the expression of MazF. To make it more convenient for future teams to use our collection, we have made a detailed description of all parts on pages in Registry.

The blue light cellulose degradation control system LightOn is so sensitive to light that as low as 15 W m-2 blue light can be sensed. The specific mechanism of this system is that when exposed to blue light (460 nm), the light sensor domain (Gal4(65)-VVD-p65 Activation Domain) can bind to its synthetic promoter (P5×UAS, 5×UAS(G)) to initiate expression of cellulase (Cex, CenA and Bglx).

The healing promoting module is used to promote wound healing and resistance to pathogens. The genes of skin growth factors EGF and bFGF were introduced into the plasmid pAAV6, and the engineered AAV infiltrated BJ cells so that BJ cells could secrete EGF and bFGF to promote skin wound healing. At the same time, the gene of human-derived antimicrobial peptide LL-37 was introduced into the plasmid pAAV6, and the engineered AAV infiltrated BJ cells, so that BJ cells could secrete LL-37 to protect against external pathogens.