한빛사 논문
Abstract
Jeongjoon Choia,1, Dongwoo Shinb,1, Hyunjin Yoona, Jiae Kima, Chang-Ro Leec, Minjeong Kima,2, Yeong-Jae Seokc, and Sangryeol Ryua,3
aDepartment of Food and Animal Biotechnology, Department of Agricultural Biotechnology, Center for Agricultural Biomaterials, and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 151-921, Korea;
bDepartment of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea; and
cDepartment of Biophysics and Chemical Biology and Institute of Microbiology, College of Natural Sciences, Seoul National University, Seoul 151-742, Korea
2Present address: Radiation Research Center for Biotechnology, Korea Atomic Energy Research Institute, Jeongeup 580-185, Korea.
Edited* by Sankar Adhya, National Cancer Institute, National Institutes of Health, Bethesda, MD, and approved October 20, 2010 (received for review January 22, 2010)
1J.C. and D.S. contributed equally to this work.
Abstract
SsrA/SsrB is a primary two-component system that mediates the survival and replication of Salmonella within host cells. When activated, the SsrB response regulator directly promotes the transcription of multiple genes within Salmonella pathogenicity island 2 (SPI-2). As expression of the SsrB protein is promoted by several transcription factors, including SsrB itself, the expression of SPI-2 genes can increase to undesirable levels under activating conditions. Here, we report that Salmonella can avoid the hyperactivation of SPI-2 genes by using ptsN-encoded EIIANtr, a component of the nitrogen-metabolic phosphotransferase system. Under SPI-2-inducing conditions, the levels of SsrB-regulated gene transcription increased abnormally in a ptsN deletion mutant, whereas they decreased in a strain overexpressing EIIANtr. We found that EIIANtr controls SPI-2 genes by acting on the SsrB protein at the posttranscriptional level. EIIANtr interacted directly with SsrB, which prevented the SsrB protein from binding to its target promoter. Finally, the Salmonella strain, either lacking the ptsN gene or overexpressing EIIANtr, was unable to replicate within macrophages, and the ptsN deletion mutant was attenuated for virulence in mice. These results indicated that normal SPI-2 gene expression maintained by an EIIANtr-SsrB interaction is another determinant of Salmonella virulence.
virulence gene regulation, nitrogen-metabolic phosphotransferase system (PTS), protein-protein interaction
Footnotes
3To whom correspondence should be addressed.
Author contributions: J.C., D.S., C.-R.L., and S.R. designed research; J.C., D.S., H.Y., J.K., C.-R.L., and M.K. performed research; J.C., D.S., H.Y., Y.-J.S., and S.R. analyzed data; and J.C., D.S., and S.R. wrote the paper.
The authors declare no conflict of interest.
*This Direct Submission article had a prearranged editor.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1000759107/-/DCSupplemental.
논문정보
관련 링크
연구자 키워드
연구자 ID
관련분야 연구자보기
소속기관 논문보기
관련분야 논문보기
해당논문 저자보기