Pathogenicity island acquisition is considered to be a costly process that in turn allows bacteria to explore new niches. While pathogenicity islands are known to be well integrated into existing regulatory networks in , we do not understand whether these islands have influenced the evolution of transcription factor coding sequence itself. Here, we exchanged two antagonisticly-acting bacterial transcription factors, RpoD (σ70) and H-NS, singly or combinatorially, between the related Gram-negative bacteria Serovar Typhimurium SL1344 and str. K12 substr. MG1655, to understand their functional divergence in relation to pathogenicity island expression in . Exchanging rpoD resulted in a small growth defect in , while exchanging hns did not. We saw a strong upregulation of pathogenicity island expression in response to rpoD exchange, while only a very weak upregulation in response to HNS exchange. Exchanging both rpoD and hns in resulted in a further upregulation of these islands. Using two different versions of the SPI1 regulatory knockout, ΔhilA and ΔhilD, where ΔhilA knocks out only SPI1 expression and ΔhilD knocks out both SPI1 and SPI2 expression, we show that both SPI1 and SPI2 expression are costly, and that their up-regulation is the cause of the growth defect in response to rpoD exchange. Thus, we show that both RpoD and H-NS sequence evolution in were geared towards constraining pathogenicity island expression, the expression cost of these islands very clearly being a driver of RpoD evolution.

  • This is an open-access article distributed under the terms of the Creative Commons Attribution License.

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