Authors: Stainier, Isabelle; Iriarte, Maite; Cornelis, Guy R.

Source: Molecular Microbiology, Volume 26, Number 4, November 1997 , pp. 833-843(11)

Publisher: Wiley-Blackwell

Abstract:

Synthesis of the Yop proteins by yersiniae is downregulated when secretion is prevented by closure or destruction of the contact (type III) secretion channel. In Yersinia pseudotuberculosis, a mutation in the lcrQ gene, encoding a secreted protein, reduces this feedback inhibition mechanism. Surprisingly, mutation in the yscM gene, the lcrQ homologue in Y. enterocolitica, does not lead to the same deregulated phenotype. In this paper, we addressed the question of this discrepancy. We found a new gene on the Y. enterocolitica pYV plasmid that encodes a protein with 57% identity to YscM (now called YscM1). Overexpression of this gene, called yscM2, like overexpression of lcrQ and yscM1, blocked Yop secretion. A double yscM1, yscM2 mutant had the same phenotype as that of the lcrQ mutant. The discrepancy can thus be explained by the existence of two functionally equivalent copies of yscM in Y. enterocolitica. Overexpression of yscM1 drastically reduced the expression of a yopH-cat reporter gene when tested in a pYV⁺ background. However, no effect could be observed in the absence of a pYV plasmid, indicating that YscM1 does not act directly as a transcriptional repressor or as an anti-VirF factor. We have also ruled out that YscM acts by obstructing the secretion channel.

Document Type: Research article

DOI: http://dx.doi.org/10.1046/j.1365-2958.1997.6281995.x

Affiliations: 1: Microbial Pathogenesis Unit, International Institute of Cellular and Molecular Pathology (ICP) and Faculté de Médecine, Université Catholique de Louvain, Avenue Hippocrate, 74, UCL 74.49, B-1200 Brussels, Belgium.

Publication date: 1997-11-01

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