Affiliation:
1. Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0620
Abstract
ABSTRACT
Legionella pneumophila
colonizes freshwater amoebae and can also replicate within alveolar macrophages. When their nutrient supply is exhausted, replicating bacteria become cytotoxic, motile, and infectious, which is thought to promote transmission to a new amoeba. The differentiation of
L. pneumophila
is coordinated by the sigma factors RpoS and FliA and the two-component regulator LetA/LetS and is enhanced by the
letE
locus. Here we demonstrate that
letE
promotes motility by increasing expression of the flagellin gene
flaA
but has little impact on the transcription of
fliA
, the flagellar sigma factor gene. In addition to promoting motility,
letE
induces the characteristic shape, pigment, and heat resistance of stationary-phase
L. pneumophila
. To gain insight into how
letE
promotes the expression of the transmission phenotype, we designed molecular genetic experiments to discriminate between the following three models:
letE
mutations are polar on
milX
;
letE
encodes a small novel protein; or, by analogy to
csrB
,
letE
encodes a regulatory RNA that sequesters CsrA to relieve repression. We report that
letE
encodes an activator protein, as it does not complement an
Escherichia coli csrB
mutant, it directs the synthesis of an ∼12-kDa polypeptide, and a
letE
nonsense mutation eliminates function. A monocistronic
letE
RNA is abundant during the exponential phase, and its decay during the stationary phase requires RpoS and LetA/LetS. We also discuss how the LetE protein may interact with LetA/LetS and CsrA to enhance
L. pneumophila
differentiation to a transmissible form.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
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