The Legionella pneumophila GacA homolog (LetA) is involved in the regulation of icm virulence genes and is required for intracellular multiplication in Acanthamoeba castellanii
There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
Legionella pneumophila, the causative agent of legionnaires' disease, is a broad-host-range
facultative intracellular pathogen. Thus far, 24 genes (icm/dot genes) required for
L. pneumophila intracellular growth, have been discovered. In this study, a deletion
substitution was constructed in the L. pneumophila homolog of the gacA response regulator
(letA) and its involvement in L. pneumophila pathogenicity and icm/dot gene expression
was characterized. The letA mutant constructed had no intracellular growth defect
when analyzed in HL-60 derived human macrophages, but it was found to be severely
attenuated for intracellular growth in the protozoan host Acanthamoeba castellanii.
The growth defect in amoebae was fully complemented by introducing the L. pneumophila
letA gene on a plasmid. In addition, the LetA regulator was found to be involved in
the expression of three icm genes (icmT, icmP and icmR). The level of expression of
the icmT::lacZ and icmR::lacZ fusions was found to be higher, while the level of expression
of the icmP::lacZ fusion was found to be lower when analyzed in the letA mutant strain,
in comparison to the wild-type strain. We concluded that LetA has a moderate effect
on icm/dot gene expression, but it probably plays a major role in the expression of
L. pneumophila genes required for intracellular growth in protozoan hosts. A similar
host specific phenotype was previously described for the RpoS sigma factor and the
type II general secretion system of L. pneumophila.
Copyright 2003 Elsevier Science Ltd.