Pycsar (pyrimidine cyclase system for antiphage resistance) provides immunity against bacteriophage. The pyrimidine cyclase (PycC) synthesizes cyclic nucleotides in response to infection; these serve as specific second messenger signals. The signals activate the adjacent effector, leading to bacterial cell death and abortive phage infection. A clade B Pycsar system. The effector gene of a two-gene Pycsar system. Expression of this and adjacent uridylate cyclase XpPycC (AC P0DV28) confers resistance to bacteriophage T7. When cells expressing the Pycsar system are infected by phage T7 at low multiplicity of infection (0.2 MOI) the culture survivey, at 2.0 MOI bacteria enter growth arrest. The same cells enter growth arrest after exposure to 2.5 mM cUMP but not cCMP; the effector protein responds only to the cUMP usually produced by its cognate NTP cyclase. NAD(+) levels in infected cells are depleted between 5 and 10 minutes after infection with T7 at MOI of 2 (PubMed:34644530). Probably only responds to cUMP (Probable). H2O + NAD(+) = ADP-D-ribose + H(+) + nicotinamide In E.coli strain MG1655 transformed with both genes NAD(+) levels fall dramatically by 10 minutes after infection with phage T7 (at protein level). Has an N-terminal cyclic nucleotide-binding domain and a C-terminal Toll/interleukin-1 receptor-like domain (TIR) that probably has the NAD(+) hydrolase activity.