lon-sulA regulatory function affects the efficiency of transposition of Tn5 from lambda b221 cI857 Pam Oam to the chromosome.

In transposition of Tn5 from lambda b221 cI857 Pam Oam rex::Tn5 to the chromosome, lon mutants of Escherichia coli K12 are less efficient than lon+ parents. Reduced frequency of transposition of Tn5 is recovered to the wild type level by adding DL-pantoyl lactone, an agent which suppresses Lon- phenotypes. A suppressor mutation, sulA (or sfiA), suppresses the deficiency of transposition as well as other known lon-associated phenotypes, whereas a lon sulB (or sfiB) double mutant is phenotypically Lon+ but still transposition-deficient. An additive effect of the sulA genes on teh chromosome and on a high copy number plasmid is found in inhibiting transposition of Tn5. A hypothesis that the SulA product someway regulates transposition of Tn5 negatively is proposed.