Hüttener Mário, Dietrich Manuela, Paytubi Sònia, Juárez Antonio
Institute for Bioengineering of Catalonia (IBEC), Barcelona, Spain.
BMC Microbiol. 2014 Oct 25;14:268. doi: 10.1186/s12866-014-0268-5.
The HilA protein is the master regulator of the Salmonella pathogenicity island 1 (SPI1). EilA and YgeH proteins show a moderate similarity to HilA and are encoded in pathogenicity islands from several E. coli strains, both pathogenic and non-pathogenic. In the present work we characterize the YgeH protein from the enteroaggregative E. coli strain 042 (locus tag EC042_3050).
We show that both E. coli 042 YgeH and EilA proteins are able to functionally replace HilA in Salmonella. Interestingly, this is not the rule for all YgeH proteins: the YgeH protein from the enterohaemorragic E. coli strain O157 appears to be non-functional. ygeH expression is not influenced by growth osmolarity or temperature, and moderately increases in cells entering the stationary phase. H-NS represses ygeH expression under all growth conditions tested, and binds with specificity to the ygeH promoter region. As expected, expression of ETT2 (Escherichia coli type 3 secretion system 2) genes requires YgeH: ETT2 operons are downregulated in a ygeH mutant. Accordingly, since H-NS represses ygeH expression, ETT2 expression is significantly increased in an hns mutant.
E. coli 042 YgeH protein is functional and able to replace HilA in Salmonella. ETT2 gene expression requires YgeH activity which, in turn, is subjected to H-NS silencing.
HilA蛋白是沙门氏菌致病岛1(SPI1)的主要调节因子。EilA和YgeH蛋白与HilA有一定程度的相似性,并且在多种致病性和非致病性大肠杆菌菌株的致病岛中编码。在本研究中,我们对肠聚集性大肠杆菌菌株042(基因座标签EC042_3050)中的YgeH蛋白进行了表征。
我们发现大肠杆菌042的YgeH和EilA蛋白在功能上都能够替代沙门氏菌中的HilA。有趣的是,并非所有的YgeH蛋白都是如此:肠出血性大肠杆菌菌株O157中的YgeH蛋白似乎没有功能。ygeH的表达不受生长渗透压或温度的影响,并且在进入稳定期的细胞中适度增加。H-NS在所有测试的生长条件下都抑制ygeH的表达,并与ygeH启动子区域特异性结合。正如预期的那样,ETT2(大肠杆菌3型分泌系统2)基因的表达需要YgeH:在ygeH突变体中ETT2操纵子被下调。因此,由于H-NS抑制ygeH的表达,ETT2的表达在hns突变体中显著增加。
大肠杆菌042的YgeH蛋白具有功能,并且能够替代沙门氏菌中的HilA。ETT2基因的表达需要YgeH的活性,而YgeH的活性又受到H-NS的沉默作用。