Functional analysis of PrsA protein of Staphylococcus aureus RN1HG

• Main Authors: Ting Kuan Zhu, 朱庭寬
• Other Authors: M. H. Lin
• Format: Others
• Published: 2013
• Online Access: http://ndltd.ncl.edu.tw/handle/90700755476974512975

碩士 === 長庚大學 === 醫學生物技術暨檢驗學系 === 101 === Staphylococcus aureus is an important community and nosocomial-associated pathogen, causing a variety of human infections including food poisoning, pneumonia, endocarditis, osteomyelitis, and sepsis. It has been shown that S. aureus is a facutative intracellular microorganism. Previous studies have demonstrated that the PrsA protein of S. aureus RN1HG significantly increased when the bacteria invaded human bronchial epithelial cells. PrsA is an extracytoplasmic lipoprotein which regulates late phase protein secretion and is involved in toxin secretion and survival in host cells. However the role of PrsA in S. aureus is not clear. To investigate the functions of PrsA in S. aureus RN1HG, we constructed a prsA knockout strain (RN1HG ΔPrsA) for exoprotein analysis, phagocytosis assay of macrophage, virulence studies using a mouse model, and SUMOylation experiments. Exoprotein analysis revealed that PrsA influences several exoproteins secretion including Alpha-hemolysin and Gamma-hemolysin component C. The results from a mouse model of intravenous infection revealed that the survival rate of mice infected with RN1HG ΔPrsA is higher than that of mice infected with the wild type RN1HG. Meanwhile, phagocytosis assay demonstrated that PrsA does not prevent phagocytosis of S. aureus by macrophage but influences the early survival of intracellular S. aureus in macrophages. In addition, this study also found that PrsA can be modified by SUMOylation which is one of posttranslational modification mechanism in eukayotes. In summary, the results from this study revealed that PrsA plays an important role in virulence and pathogenesis of S. aureus. PrsA may enhance early survival of intracellular S. aureus in macrophage. This study also found that PrsA is a target protein for SUMOylation.