초록 ▼

- 본 연구는 해양세균에 의한 생물막형성에 대한 체계적인 이해를 도모하고자, 해양모델세균의 생물막형성 조절체계를 부착-성숙-전이 단계별로 규명하며, 단계별 중요인자 및 그 조절체계의 교란을 통한 항생물막 기전을 개발함으로써, 기존의 미생물 제어/조절 방법과는 다른 차원의 미생물 제어방안을 마련하고자 함.
- 이를 위하여, 제1단계에서는 군집/개체군 수준 그리고 세포/분자 수준에서 다각도의 연구를 수행하여 생물막 세균군집의 특성 및 생물막 형성 신호전달체계의 기작을 이해하고; 제2단계에서는 해양모델세균의 생물막 구성인자의 특성

- 본 연구는 해양세균에 의한 생물막형성에 대한 체계적인 이해를 도모하고자, 해양모델세균의 생물막형성 조절체계를 부착-성숙-전이 단계별로 규명하며, 단계별 중요인자 및 그 조절체계의 교란을 통한 항생물막 기전을 개발함으로써, 기존의 미생물 제어/조절 방법과는 다른 차원의 미생물 제어방안을 마련하고자 함.
- 이를 위하여, 제1단계에서는 군집/개체군 수준 그리고 세포/분자 수준에서 다각도의 연구를 수행하여 생물막 세균군집의 특성 및 생물막 형성 신호전달체계의 기작을 이해하고; 제2단계에서는 해양모델세균의 생물막 구성인자의 특성 및 이물질의 방오후보물질로서의 유용성을 파악하고; 제3단계에서는 모델세균의 생물막형성 조절체계를 부착-성숙-전이 단계별로 규명하고 각 단계별 핵심인자 및 그 조절체계의 교란을 통한 항생물막 기전을 개발함.
- 이러한 연구를 통하여, 해양세균 생물막 형성을 다음의 수준에서 이용, 활용함.
1. 해양세균의 생물막형성의 특징 규명
2. 해양세균의 생물막형성 핵심인자의 특성 및 합성조절 기작 규명
3. 해양세균의 생물막 단계별 형성 조절체계 규명
4. 해양세균의 생물막형성 교란/제어 기전 이해

Abstract ▼

Since A. van Leeuwenhoek first observed a surface-associated multicellular structure of bacterial cells in the 17th century, it has been shown to exhibit an ability to form a biofilm by numerous bacterial species. Bacteria show surface-associated life styles in multicellular structures, which provid

Since A. van Leeuwenhoek first observed a surface-associated multicellular structure of bacterial cells in the 17th century, it has been shown to exhibit an ability to form a biofilm by numerous bacterial species. Bacteria show surface-associated life styles in multicellular structures, which provide advantages in their survival against diverse environmental stresses. Specifically, the abilities of pathogenic bacteria to form multicellular structures on surfaces facilitate their host invasion via mediating adherence to host tissues and evasion from host defense mechanisms (Costerton et al., 1995). A mature biofilm is composed of aggregated microbial cells surrounded by a self-produced extracellular polymeric matrix (EPM) (Sutherland, 2001). A model marine bacterial species, Vibrio vulnificus, a human pathogen causing fatal septicemia, exhibits an ability to form biofilms and its pathogenicity correlates with biofilm formation ability. We have demonstrated that the global transcription regulator NtrC and its cognate alternative sigma factor, RpoN, are essential in biofilm formation via modulating gene expression of gmhD , of which the gene product constitutes biosynthetic enzymes for lipo polysaccharide (LPS) biosynthesis (Kim et al., 2007). Interestingly, the gmhD mutation also resulted in a partial defect in exopolysaccharide (EPS) production. Therefore, we further studied the roles of EPS in biofilm formation by examining the phenotypes of various EPS-deficient mutants and the expression patterns of three EPS-related gene clusters. V vulnificus has been shown to require a global transcription factor, NtrC for mature biofilm development via controlling the biosyntheses of LPS and EPS. The regulatory roles of NtrC in EPS biosynthesis were studied with three gene clusters for EPS biosyntheses. Transcriptions of the three clusters were positively controlled by NtrC and showed maximal expression at the early stage of biofilm development. Mutants deficient in one of three EPS syntheses showed decreased production of EPS, attenuated ability to form biofilm, and lowered cytoadherence to human epithelial cells. These results demonstrate that NtrC-regulated EPS are crucial in biofilm formation of V. vulnificus, and some EPS components play important roles in interacting with hosts (Kim et al., 2009). V vulnificus extracellular matrix also includes capsular polysaccharide (CPS), a determinant of colony opacity. A CPS-deficient mutant formed enlarged biofilms compared to wildtype, due to increased hydrophobicity of cell surface and thus altered abilities to adhere to surfaces.
The mutant exhibited increased adherence to abiotic surfaces and produced highly aggregated cell masses. This process should be followed by the maturation stage at which cell densities reach high. Thus, it was investigated whether CPS biosynthesis is dependent upon quorum-sensing (QS) regulation and found the cps-cluster transcription was activated by a QS master regulator. Therefore, CPS of V. vulnificus, produced once biofilm cell densities reach high enough to turn on QS regulation, limits the biofilm structure (Lee et al., 2013).