Enteroaggregative (EAEC) is an pathotype associated with diarrhea and growth faltering. EAEC virulence gene expression is controlled by the autoactivated AraC family transcriptional regulator, AggR. AggR activates transcription of a large number of virulence genes, including Aar, which in turn acts as a negative regulator of AggR itself. Aar has also been shown to affect expression of housekeeping genes, including H-NS, a global regulator that acts at multiple promoters and silences AT-rich genes (such as those in the AggR regulon). Although Aar has been shown to bind both AggR and H-NS , functional significance of these interactions has not been shown In order to dissect this regulatory network, we removed the complex interdependence of and by placing the genes under the control of titratable promoters. We measured phenotypic and genotypic changes on downstream genes in EAEC strain 042 and K-12 strain DH5α, which lacks the AggR regulon. In EAEC, we found that low expression of increases fimbrial gene expression via H-NS; however, when is more highly expressed, it acts as a negative regulator via AggR. In DH5α, affected expression of genes in some cases via H-NS and in some cases independent of H-NS. Our data support the model that Aar interacts in concert with AggR, H-NS, and possibly other regulators and that these interactions are likely to be functionally significant .

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240098PMC
http://dx.doi.org/10.1128/IAI.00100-20DOI Listing

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