[Minor promoters of phage phi X174 are controlled by CRP-cAMP, lexA, glnG and several other common common regulatory systems of the host cell].

It was found that CRP-cAMP-recognized sequences in DNA being suggested as GTGN7-11CAC (with variability both in domain's structures and in spacer's length) are located non-randomly in promoters. In CRP-cAMP-stimulated promoters they lie upstream the "-35" box and are separated from it by a whole number of DNA turns, whereas in CRP-cAMP-repressed ones they are located downstream "-35" in a half-whole-turn-number distance. Several CRP-, SOS- and NR1-sites in the phi X174 DNA sequence were found and a few new promoters were deduced from it. PCRP1 lies within gene F and has both CRR and ntrC sites and one SOS-operator, PCRP3 (in gene A) has a CRP site which overlaps with the SOS-operator, PA and PCRP2 (in gene G) have sCRP and PD has a stringent discriminator. Four promotors, PCRP1, PCRP2, PA and PB are cloned in the pBR322 plasmid. For cloned PCRP1 the activation by exogenous cAMP and the SOS-induction by the mitomycin C were observed in vivo in pVYB215-containing cells by increasing the levels of beta-lactamase up to 27-fold. The new gene L of the phi X174 is deduced from the DNA sequence. It has two start points, overlaps the gene F inside it and codes for peptides 23 or 19 amino acids in length. These lethal peptides have strong homology in sequence to the cellular protein sulA(sfiA) of E. coli, and L* can cause observed filamentation and death of pVYB215- bearing cells after PCRP1 induction. In the A and A* protein sequences two domains "helix-turn-helix" were found that are homologous to those in CRP and repressors; this makes possible the competition between A* and CRT for its DNA sites that also have some homology. The model of the phi X174 infection cycle control and mechanisms of DNA recognition by CRP-CAMP are discussed. PCRP1 is the first promotor controlled by both three global regulons of E. coli cell.