Open AccessThe Salmonella Typhimurium InvF-SicA complex is necessary for the transcription of sopB in the absence of the repressor H-NS
Author(s) -
Luis E. Romero-González,
Deyanira Pérez-Morales,
Daniel Cortés-Avalos,
Edwin Vázquez-Guerrero,
Denisse A. Paredes-Hernández,
Paulina Estrada-de los Santos,
Lourdes VillaTanaca,
Miguel A. De la Cruz,
J. Antonio Ibarra
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0240617
Subject(s) - derepression , repressor , salmonella enterica , biology , gene , transcription factor , pathogenicity island , gene expression , regulation of gene expression , microbiology and biotechnology , virulence , salmonella , dna , transcription (linguistics) , psychological repression , genetics , escherichia coli , bacteria , linguistics , philosophy
Expression of virulence factors in non-typhoidal Salmonella enterica depends on a wide variety of general and specific transcriptional factors that act in response to multiple environmental signals. Expression of genes for cellular invasion located in the Salmonella pathogenicity island 1 (SPI-1) is tightly regulated by several transcriptional regulators arrayed in a cascade, while repression of this system is exerted mainly by H-NS. In SPI-1, H-NS represses the expression mainly by binding to the regulatory region of hilA and derepression is exercised mainly by HilD. However, the possible regulatory role of H-NS in genes downstream from HilD and HilA, such as those regulated by InvF, has not been fully explored. Here the role of H-NS on the expression of sopB , an InvF dependent gene encoded in SPI-5, was evaluated. Our data show that InvF is required for the expression of sopB even in the absence of H-NS. Furthermore, in agreement with previous results on other InvF-regulated genes, we found that the expression of sopB requires the InvF/SicA complex. Our results support that SicA is not required for DNA binding nor for increasing affinity of InvF to DNA in vitro . Moreover, by using a bacterial two-hybrid system we were able to identify interactions between SicA and InvF. Lastly, protein-protein interaction assays suggest that InvF functions as a monomer. Derived from these results we postulate that the InvF/SicA complex does not act on sopB as an anti-H-NS factor; instead, it seems to induce the expression of sopB by acting as a classical transcriptional regulator.