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The experiment shows seven classes where the mice are exposed to one of three microbes at both 4 and 24 h; FTN, Pseudomonas aeruginosa (PA), or an avirulent strain of FTN that contains a mutation to the transcriptional regulator mglA (MGLA).
and its regulator mglA [9], [10].
Additionally, the transcriptional regulator MglA was upregulated during stationary phase growth in the hfq mutant.
The transcriptional regulator mglA plays a crucial role in phagosomal escape.
novicida), and Pseudomonas aeruginosa were used along with a non-pathogenic mutant of F. novicida that lacks the transcriptional regulator mglA.
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The FPI genes, as well as the mglA global regulator, are required for modulation of phagosome biogenesis and escape into the cytosol of human-derived and D. melanogaster-derived cells [22], [23].
It has been demonstrated that the F. tularensis stress response required for its survival in diverse hostile environments is dependent on the MglA transcriptional regulator of genes contributing to virulence by encoding the Francisella pathogenicity island [ 15].
Regulator-regulated gene associations.
The Frz system regulates cell polarity through MglA, a Ras family GTPase.
Finally, through genome-wide expression analyses, we demonstrate that MglA and SspA regulate the same set of genes.
The MglA protein is the only known regulator of virulence gene expression in Francisella tularensis, yet it is unclear how it functions.
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