Open AccessContribution of the Rgg Transcription Regulator to Metabolism and Virulence of Streptococcus suis Serotype 2
Author(s) -
Zijian Feng,
Hongfeng Ji,
Min Cao,
Changjun Wang,
Youjun Feng,
Ming Li,
Xiuzhen Pan,
Jing Wang,
Yue-Hong Qin,
Fuquan Hu,
Jiaqi Tang
Publication year - 2011
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00193-10
Subject(s) - biology , virulence , gene , streptococcus suis , transcriptional regulation , dna microarray , regulator , pathogen , microbiology and biotechnology , genetics , transcription (linguistics) , response regulator , regulation of gene expression , phenotype , transcription factor , gene expression , mutant , linguistics , philosophy
The Rgg-like regulators, a family of transcription factors commonly found in many Gram-positive bacteria, play multiple roles, especially in the control of pathogen virulence. Here, we report anrgg homologue from a Chinese isolate, 05ZYH33, ofStreptococcus suis serotype 2 (SS2). Deletion of thergg gene in SS2 increased its adhesion to Hep-2 cells and hemolytic activityin vitro . Significantly, inactivation of thergg gene attenuated SS2 virulence in an experimental piglet infection model. Using DNA microarrays and quantitative reverse transcription-PCR, we found that the Rgg regulator affects the transcriptional profile of 15.87% (n = 345) of all of the annotated chromosomal genes, including those involved in nonglucose carbohydrate metabolism, DNA recombination, protein biosynthesis, bacterial defense mechanisms, and others. It was experimentally verified that the deletion ofrgg in SS2 reduced the utilization of nonglucose carbohydrates, such as lactose and maltose. In addition, thergg gene was found to be associated with changes in the bacterial microscopic phenotype and growth curve. These data suggested that Rgg in SS2 is a global transcriptional regulator that plays an important role in promoting SS2 bacterial survival during pathogen-host interaction.