Homing endonuclease genes are mobile elements that promote their duplication into cognate sites of genomes that lack the endonuclease gene. The encoded homing endonuclease initiates this event through site-specific DNA cleavage. Copying of the endonuclease gene follows as a consequence of DNA repair. I characterized a novel endonuclease, F-CphI from cyanobacteriophage S-PM2. It is encoded by the gene orf177, which is inserted between the photosynthesis genes psbA (which contains a group I intron) and psbD. The psbAD region of the closely related phage S-BM4 lacks both an intron and orf177. Endonuclease F-CphI makes a specific double-strand cut near the intron insertion site of S-BM4 psbA, its DNA recognition site spans the intron insertion site, and it is unable to cleave the intron-containing S-PM2 psbA gene. This interdependence of a free-standing endonuclease gene and a group I intron, which we denote collaborative homing, has not been reported previously and gives support to a hypothesis of formation of composite mobile introns by independent convergence of an intron and an endonuclease gene on the same target sequence. I purified F-CphI and determined some of its basic biochemical properties. F-CphI is highly similar to endonucleases VII (Endo VII), the DNA resolvase of bacteriophage T4. Site-directed mutagenesis confirmed that conserved residues essential for Endo VII were also essential for F-CphI. F-CphI may represent a new family of homing endonuclease that utilizes the catalytic domain of Endo VII for DNA cleavage. I also found a situation similar to collaborative homing, in phage T4 gene 39-60 region. While the large subunit topoisomerase gene 39 of T2 is a continuous open reading frame, gene 39 of T4 is split by MobA insertion into two independent cistrons, genes 39 and 60. T4 gene 60 contains a 50 nt translational bypass sequence that is present in the mRNA, but is skipped by ribosomes during translation. Similar to collaborative homing, the bypass sequence in T4 gene 60 prevents cleavage by MobA. MobA and the bypass sequence form a mobile module that can transfer to phage T2 by cleaving its gene 60, which doesn't have the bypass sequence.