“…When supplied in trans , helicase‐inactive priA alleles with mutations in the Walker box nucleotide binding motif ( priA K230R , priA K230A and priA K230D ) restore apparently wild‐type levels of viability and cell morphology to priA null strains (Zavitz and Marians, 1992; Kogoma et al ., 1996; Sandler et al ., 1996; Masai et al ., 1999). Two of these alleles allow strains to assimilate genetic markers by homologous recombination, albeit at 30–50% of the level of wild type (Zavitz and Marians, 1992; Kogoma et al ., 1996; Sandler et al ., 1996), while the third, priA K230D , supports only low levels of iSDR (Masai et al ., 1999). Work in the Mu system suggests a role for the helicase and also indicates that other proteins in the cell can compensate for the lack of PriA helicase activity (Jones and Nakai, 1999).…”