Antitermination increases the transcription of genes that are located downstream of terminators. Transcripts encoded by the cis-acting antitermination sites (put sites) of lambdoid phage HK022 promote readthrough of downstream transcription terminators. Proper conformation of the transcripts is essential for activity, since put mutations that prevent the formation of predicted RNA stems prevented antitermination, and suppressor mutations that restore the stems restored antitermination. Antitermination does not appear to require proteins other than RNA polymerase, since put-dependent readthrough of multiple sequential terminators was observed in a purified transcription system containing only template, polymerase, substrates, buffer, and product. Transcription of put also increased the elongation rate of polymerase, very likely by suppressing pausing. A mutation that alters the zinc-finger region of the beta' subunit of polymerase specifically prevented the put-dependent increases in terminator readthrough and elongation rate. The simplicity of HK022 antitermination contrasts with that of other known antitermination pathways. We propose that the central effector is a transcript that directly alters the elongation properties of RNA polymerase. The integrase proteins of phages lambda and HK022 are closely related site-specific recom binases that recognize different nucleotide sequences in the core regions of their substrates, the att achment sites of the two phages. We have now identified several attachment site nucleotides that inhibit recombination by the non-cognate integrase. These include G4 in the lambda B' core site and A1 and C3 in the HK022 B' and C core sites. Interestingly, nucleotides flanking the canonical core sites also appear to be recognized by integrase.
