The (+) ssDNA of classical variants of CTXφ recombines with both dif1 and dif2. (A) The three categories of phage attachment regions found in CTXφ variants. Residues specifically conserved in classical and G variants of the phage are shown in blue and red, respectively. (B) Schemes of Watson–Crick bp interactions that could stabilize the strand exchange catalyzed by XerC between the overlap regions of the two dimer resolution sites of N16961 and the attachment site found in the (+) ssDNA genome of classical variants of CTXφ. The legend is as in Fig. 1C. (C) V. cholerae XerCD-mediated recombination of attP^ET(+) with dif1 and dif2. A short radioactively labeled attP substrate was reacted with a longer cold dimer resolution substrate (Left Panels), and a short radioactively labeled dimer resolution substrate was reacted with a longer cold attP substrate (Right Panels). Schemes of substrate and products are indicated on the side of each panel. A black triangle indicates the position of cleavage of V. cholerae XerC. A star indicates the position of the radioactive label of the probe. (D) V. cholerae XerCD-mediated recombination of attP^Cl(+) with dif1 and dif2. Schemes of the products and of the substrate are indicated as in Fig. 2B.

Lysogenic conversion of V. cholerae strains by CTXφ. (A) CTXφ variants found in cholera epidemic strains. V. cholerae strains: gray, unknown; blue, classical; black, El Tor; green, O139. CTXφ variants: gray, unknown; blue, classical; black, El Tor; green, O139; red, G; black and blue, El Tor and classical hybrid. (B) Scheme of Xer recombination sites. dif1, dimer resolution site of the N16961 chromosome 1; attP1 and attP2, Xer sites found in the replicative form of CTXφ (pCTXφ); attP(+), the recombination site created by the folding of the (+) ssDNA genome of CTXφ. The two DNA strands of each site are drawn. The strand cleaved by XerC is shown in color. Vertical bars indicate bases present in the overlap region of each site. (C) Schemes of the Watson–Crick bp interactions that could stabilize the strand exchange catalyzed by XerC between the overlap regions of the two chromosome dimer resolution sites of N16961 and the two putative attachment sites of El Tor variants of CTXφ. dif1, chromosome 1 dimer resolution site; dif2, chromosome 2 dimer resolution site; attP1^ET, attP1 found in CTXφ El Tor variants; attP(+)^ET, attachment site unmasked by the folding of the (+) ssDNA genome of El Tor variants of CTXφ. The strands cleaved by XerC on dimer resolution and phage attachment sites are shown in red and in blue, respectively. Pairing interactions are indicated by the proximity of the bases.

Homology determinants implicated in lysogenic conversion. (A) Design of a variant of CTXφ specifically integrating at dif2. The legend is as in Figs. 1C and 2C. (B) Scheme showing the possible pairing interactions between difG and attP^ET(+) or attP^Cl(+). The legend is as in Fig. 1C. (C) V. cholerae XerCD-mediated recombination of attP^G(+) with dif1, dif2, and difG. A scheme of the possible pairing interactions is shown above the gels. The legend is as in Figs. 1C and 2C.