Yinduo Ji , Ph.D Associate Professor Veterinary and Biomedical Sciences Chinese Academy of Preventive Medicine, 1993, Ph.D. jixxx002@umn.edu office - 612-624-2757 lab - 612-624-5349

Research Interests:

Molecular pathogenesis of staphylococcal infection

Staphylococcus aureus is a major community- and hospital-acquired pathogen that can cause severe infections, including pneumonia, endocarditis, and sepsis. This organism has evolved a series of two-component signal transduction systems in order to sense its immediate surroundings and to modulate cellular responses and the expression of virulence genes. One project is to investigate the regulatory mechanisms of different two-component signal transduction systems, such as yhcSR, yycFG, saeRS, and arlRS, for bacterial survival and/or infection. Another project is to determine biological function of critical unknown genes, such as gcp, for bacterial growth and pathogenesis and monitoring of host cell gene expression during host-pathogen interaction and apoptosis. These efforts will provide new insight into molecular mechanism of pathogenesis as well as may deliver unexploited targets for developing preventive and/or therapeutic agents against this life-threatening pathogen and benefit public health. Molecular genetic, antisense RNA, microarray, genomics, proteomics, cell culture, immunochemical, and sophisticated imaging methods are used in these studies.

Selected Recent Publications:

• Liang X., J. Yang, and Y. Ji. 2009. The H35A mutated alpha-toxin interferes with cytotoxicity of staphylococcal alpha-toxin. Infect. Immun. 77:977-983.
• Yan M., C. Yu, J, Yang, L. Zhang, and Y. Ji. 2009. Development of shuttle vectors for evaluation of essential gene regulation in Staphylococcus aureus. Plasmid 61:188-192.
• Yin D. and Y. Ji. 2008. Identification of essential genes in Staphylococcus aureus by construction and screening of conditional mutant library. Methods Mol. Biol. 416:297-305.
• Liang X. and Y. Ji. 2007. Involvement of 5alpha 1beta-integrin and TNF-alpha in Staphylococcus aureus alpha-toxin-induced death of epithelial cells. Cell. Microbiol. 9. Published article online: 14-Mar-2007.
• Zheng L., C. Yu, K. Bayles, I. Lasa, and Y. Ji. 2007. Conditional mutation of an essential putativeglycoprotease eliminates autolysis in Staphylococcus aureus. J. Bacteriol. 189:2734-2742.
• Liang X. and Y. Ji. 2006. Alpha-toxin interferes with integrin-mediated adhesion and internalization of Staphylococcus aureus by human lung epithelial cells. Cell. Microbiol. 8: 1656-1668.
• Liang X., C. Yu, J. Sun, H. Liu, C. Landwehr, D. Holmes, and Y. Ji. 2006. Inactivation of a two-component signal transduction system, SaeRS, eliminates adhesion and attenuates virulence of Staphylococcus aureus. Infect. Immun. 74: 4655-4665.
• Sun J., L. Zheng, C. Landwehr, J. Yang, and Y. Ji. 2005. Identification of a novel essential two-component signal transduction system, YhcSR, in Staphylococcus aureus.
  J. Bacteriol. 187: 7876-7880.
• Liang, X., L. Zheng, C. Landwehr, D. Lunsford, D. Holmes, and Y. Ji. 2005. Global regulation of gene expression by ArlRS, a two- component signal transduction regulatory system in Staphylococcus aureus. J. Bacteriol.187:5486-5492.
• Yin, D., F. Brian, M. Lonetto, M.R. Etherton, D. Payne, D. Holmes, M. Rosenberg, and Y. Ji. 2004. Identification of antimicrobial targets using a comprehensive genomic approach. Pharmacogenomics 5:101-113.
• Burnham, M., and Y. Ji. 2004. Antisense peptide nucleic acids in antibacterial drug discovery. Molecular Therapy. 10:614-615.
• Yin, D., and Y. Ji. 2002. Genomic analysis using conditional phenotypes generated by antisense RNA. Current Opinion in Microbiology 5:330-333.
• Ji, Y., B. Zhang, S. Van Horn, P. Warren, M. Burnham, G. Woodnutt, and M. Rosenberg. 2001. Identification of critical staphylococcal genes using conditional growth phenotypes generated by antisense RNA. Science 293:2266-2269.

   

Last modified on: August 10, 2009