In Salmonella enterica, the pathogenicity island 2 (SPI-2) regulator
PagR regulates its own expression and the expression of a five-gene
operon that encodes transketolase C
Abstract
The enteropathogen Salmonella enterica subsp. enterica sv.
Typhimurium str. LT2 (hereafter S. Typhimurium) utilizes a
cluster of genes encoded within the pathogenicity island 2 (SPI-2) of
its genome to proliferate inside macrophages. The expression of SPI-2 is
controlled by a complex network of transcriptional regulators and
environmental cues, which now include a recently characterized
DNA-binding protein named PagR. Growth of S. Typhimurium in low
phosphate low magnesium medium mimics conditions inside macrophages.
Under such conditions, PagR ensures SPI-2 induction by upregulating the
transcription of slyA, a known activator of SPI-2. Here we report
that PagR represses the expression of a divergently transcribed
polycistronic operon that encodes the two subunits of transketolase TktC
( i.e., tktD, tktE) of this bacterium. Transketolases contribute
to the non-redox rearrangements of phosphorylated sugars of the pentose
phosphate pathway, which provide building blocks for amino acids,
nucleotides, cofactors, etc. We also demonstrate that PagR represses the
expression of its own gene and define two PagR binding sites between
stm2344 and pagR.