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H-NS represses inv transcription in Yersinia enterocolitica through competition with RovA and interaction with YmoA.
J Bacteriol. 2006 Jul; 188(14):5101-12.JB

Abstract

Yersinia enterocolitica is able to efficiently invade Peyer's patches with the aid of invasin, an outer member protein involved in the attachment and invasion of M cells. Invasin is encoded by inv, which is positively regulated by RovA in both Y. enterocolitica and Yersinia pseudotuberculosis while negatively regulated by YmoA in Y. enterocolitica and H-NS in Y. pseudotuberculosis. In this study we present data indicating H-NS and RovA bind directly and specifically to the inv promoter of Y. enterocolitica. We also show that RovA and H-NS from Y. enterocolitica bind to a similar region of the inv promoter and suggest they compete for binding sites. This is similar to recently published data from Y. pseudotuberculosis, revealing a potentially conserved mechanism of inv regulation between Y. enterocolitica and Y. pseudotuberculosis. Furthermore, we present data suggesting H-NS and YmoA form a repression complex on the inv promoter, with H-NS providing the binding specificity and YmoA interacting with H-NS to form a repression complex. We also demonstrate that deletion of the predicted H-NS binding region relieves the requirement for RovA-dependent transcription of the inv promoter, consistent with RovA acting as a derepressor of H-NS-mediated repression. Levels of H-NS and YmoA are similar between 26 degrees C and 37 degrees C, suggesting that the H-NS/YmoA repression complex is present at both temperatures, while the levels of rovA transcript are low at 37 degrees C and high at 26 degrees C, leading to expression of inv at 26 degrees C. Expression of RovA at 37 degrees C results in transcription of inv and production of invasin. Data presented here support a model of inv regulation where the level of RovA within the cell governs inv expression. As RovA levels increase, RovA can successfully compete for binding to the inv promoter with the H-NS/YmoA complex, resulting in derepression of inv transcription.

Authors+Show Affiliations

Washington University School of Medicine, Department of Molecular Microbiology, 660 S. Euclid Ave., Campus Box 8230, St. Louis, MO 63110, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16816182

Citation

Ellison, Damon W., and Virginia L. Miller. "H-NS Represses Inv Transcription in Yersinia Enterocolitica Through Competition With RovA and Interaction With YmoA." Journal of Bacteriology, vol. 188, no. 14, 2006, pp. 5101-12.
Ellison DW, Miller VL. H-NS represses inv transcription in Yersinia enterocolitica through competition with RovA and interaction with YmoA. J Bacteriol. 2006;188(14):5101-12.
Ellison, D. W., & Miller, V. L. (2006). H-NS represses inv transcription in Yersinia enterocolitica through competition with RovA and interaction with YmoA. Journal of Bacteriology, 188(14), 5101-12.
Ellison DW, Miller VL. H-NS Represses Inv Transcription in Yersinia Enterocolitica Through Competition With RovA and Interaction With YmoA. J Bacteriol. 2006;188(14):5101-12. PubMed PMID: 16816182.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - H-NS represses inv transcription in Yersinia enterocolitica through competition with RovA and interaction with YmoA. AU - Ellison,Damon W, AU - Miller,Virginia L, PY - 2006/7/4/pubmed PY - 2006/8/22/medline PY - 2006/7/4/entrez SP - 5101 EP - 12 JF - Journal of bacteriology JO - J Bacteriol VL - 188 IS - 14 N2 - Yersinia enterocolitica is able to efficiently invade Peyer's patches with the aid of invasin, an outer member protein involved in the attachment and invasion of M cells. Invasin is encoded by inv, which is positively regulated by RovA in both Y. enterocolitica and Yersinia pseudotuberculosis while negatively regulated by YmoA in Y. enterocolitica and H-NS in Y. pseudotuberculosis. In this study we present data indicating H-NS and RovA bind directly and specifically to the inv promoter of Y. enterocolitica. We also show that RovA and H-NS from Y. enterocolitica bind to a similar region of the inv promoter and suggest they compete for binding sites. This is similar to recently published data from Y. pseudotuberculosis, revealing a potentially conserved mechanism of inv regulation between Y. enterocolitica and Y. pseudotuberculosis. Furthermore, we present data suggesting H-NS and YmoA form a repression complex on the inv promoter, with H-NS providing the binding specificity and YmoA interacting with H-NS to form a repression complex. We also demonstrate that deletion of the predicted H-NS binding region relieves the requirement for RovA-dependent transcription of the inv promoter, consistent with RovA acting as a derepressor of H-NS-mediated repression. Levels of H-NS and YmoA are similar between 26 degrees C and 37 degrees C, suggesting that the H-NS/YmoA repression complex is present at both temperatures, while the levels of rovA transcript are low at 37 degrees C and high at 26 degrees C, leading to expression of inv at 26 degrees C. Expression of RovA at 37 degrees C results in transcription of inv and production of invasin. Data presented here support a model of inv regulation where the level of RovA within the cell governs inv expression. As RovA levels increase, RovA can successfully compete for binding to the inv promoter with the H-NS/YmoA complex, resulting in derepression of inv transcription. SN - 0021-9193 UR - https://www.unboundmedicine.com/medline/citation/16816182/H_NS_represses_inv_transcription_in_Yersinia_enterocolitica_through_competition_with_RovA_and_interaction_with_YmoA_ L2 - http://jb.asm.org/cgi/pmidlookup?view=long&pmid=16816182 DB - PRIME DP - Unbound Medicine ER -