Pathogenic organisms inhabit one of several defined locations within a
host where temperature, pH, and nutrients are relatively constant. Wh
ile the microorganism must adapt to different environments within the
host, the host immune system is the most formidable predator that can
limit the growth of a pathogen, Neisseria gonorrhoeae (the gonococcus,
Gel is the causative agent of gonorrhoea, and has evolved several sys
tems for varying the antigenicity of different surface antigens, presu
mably to help evade the effects of the human immune system. The On/Off
/On phase variation of surface structure expression also alters the an
tigenic characteristics of the bacterial cell surface. Antigenic varia
tion of the major subunit of the pilus, pilin, occurs by unidirectiona
l, homologous recombination between a silent locus and the expression
locus. The silent loci lie from 1 to 900 kb from the expression locus
in the chromosome yet all can donate their sequences to the expression
locus. The genetic composition of the pilin loci of two Gc strains ha
s been elucidated, and the types of changes that lead to altered forms
of the pilus have been extensively characterized. However, little is
known about the precise molecular mechanisms used to allow high-freque
ncy, non-reciprocal, chromosomal recombination between pilin loci or a
bout what regulates the process of maintaining chromosome fidelity.