Abstract
Switching between the pathogenic smooth (1116S) and nonpathogenic rough (1116R) forms of
Pseudomonas tolaasii
occurs due to the reversible duplication of a 661-bp element within the
pheN
locus. Disruption of the chromosomal
recA
locus of 1116S and 1116R produced strains 1116S
recA
and 1116R
recA
, respectively, which showed typical loss of UV resistance. Switching from the smooth to the rough form was virtually eliminated in the 1116S
recA
strain, whereas the extent of switching from the rough to the smooth form was almost identical in 1116R and 1116R
recA
. It is concluded that phenotypic switching from 1116S to 1116R is
recA
dependent whereas that from 1116R to 1116S is
recA
independent.