Regulation of the Type I-F CRISPR-Cas system by CRP-cAMP and GalM controls spacer acquisition and interference

摘要: The CRISPR-Cas prokaryotic ‘adaptive immune systems’ represent a sophisticated defence strategy providing bacteria and archaea with protection from invading genetic elements, such as bacteriophages or plasmids. Despite intensive research into their mechanism application, how systems are regulated is less clear, nothing known about the regulation of Type I-F systems. We used Pectobacterium atrosepticum, Gram-negative phytopathogen, to study regulation, since it contains single system. CRP-cAMP complex activated cas operon, increasing expression adaptation genes cas1 cas2–3 in addition encoding Csy surveillance complex. Mutation crp cyaA (encoding adenylate cyclase) resulted reductions both primed spacer acquisition interference. Furthermore, we identified galactose mutarotase, GalM, which reduced operon CRP- CyaA-dependent manner. propose that system senses metabolic changes, sugar availability, regulates initiate an appropriate response. Indeed, elevated glucose levels Taken together, these findings highlight metabolite-sensing regulatory pathway controls modulate