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MOLECULAR BIOLOGY OF FUSOBACTERIUM ADHERENCE

MOLECULAR BIOLOGY OF FUSOBACTERIUM ADHERENCE
梭杆菌粘附的分子生物学
批准号:
2132346
负责人:
SUSAN KINDER HAAKE
金额:
$3.83万
依托单位国家:
美国
项目类别:
财政年份:
1994
资助国家:
美国
项目状态:
已结题
起止时间:
1994-09-01 至 1996-08-31

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中文摘要
翻译
牙周病是最常见的传染病之一, 是成年人牙齿脱落的主要原因。的能力 牙周病原体,如革兰氏阴性杆菌 有核细菌和牙龈卟啉单胞菌,能附着在其他菌斑上 微型橘子被认为是殖民过程中必不可少的,因此 感染过程中的关键事件。核镰刀菌T18附着于P. 牙周病毒T22和主要外膜蛋白APG(黏附于 牙龈卟啉单胞菌),被认为是一种粘连 互动。这项调查中要检验的假设是 APG在核镰刀菌T18的黏附中起着黏附作用 至牙龈假单胞菌T22。为了检验这一假设,第一个问题 需要解决的问题是:F. 核仁形成是由apg突变引起的吗?我们建议建造一个 穿梭诱变核盘藻T18的APG突变体。这个APG- 突变体的特征,包括对表达的检查 APG和粘附性。基因插入失活 是鉴定基因产物功能的有力工具,但 重要的是要排除产生极地效应的可能性。 从基因的破坏中。因此,需要解决的第二个问题 IS:粘连缺陷(A-)APG突变体的互补 有了意志型APG轨迹,就会回归到坚守- 有效的(A+)表型?将进行互补研究 使用A-、apg-突变体和即将开发的质粒载体 核盘藻F.nuatum. 这些研究将加深我们对分子基础的理解。 F.成核菌-牙龈假单胞菌黏附,并提供工具 对于进一步研究解决殖民问题和 核假单胞菌和牙龈假单胞菌的致病机制。另外, 这项研究涉及到操纵系统的开发, 将是研究任何一种 核盘藻和其他可能相关的革兰氏菌的表型特性 厌氧菌阴性。
英文摘要
Periodontal diseases are among the most common infectious diseases and constitute a major cause of tooth loss in adults. The ability of periodontal pathogens, such as the gram-negative species Fusobacterium nucleatum and Porphyromonas gingivalis, to adhere to other plaque microorangisms is though to be essential in colonization, and thus a key event in the infectious process. F. nucleatum T18 adheres to P. gingivalis T22 and the major outer membrane protein, Apg (Adherence to Porphyromonas Gingivalis), has been implicated as an adhesion in this interaction. The hypothesis to be tested in this investigation is that Apg functions as an adhesion in the adherence of F. nucleatum T18 to P. gingivalis T22. To examine this hypothesis, the first question to be addressed is: Do adherence-defective (A-) mutants of F. nucleatum result from a mutation in apg? We propose to construct an apg- mutant of F. nucleatum T18 using shuttle mutagenesis. The apg- mutant will be characterized, including examination of the expression of Apg and adherence properties. Insertional inactivation of a gene is a powerful tool to identify the function of the gene product, but it is important to rule out the possibility of polar effects resulting from the gene disruption. Thus the second question to be addressed is: Does complementation of an adherence-defective (A-) apg- mutant with the will type apg locus result in reversion to the adherence- effective (A+) phenotype? Complementation studies will be performed using the A-, apg- mutant and a plasmid vector that will be developed F. nucleatum. These studies will enhance our understanding of the molecular basis of F. nucleatum - P. gingivalis adherence, and provide the tools essential for further studies addressing the colonization and pathogenesis of both F. nucleatum and P. gingivalis. Additionally, this research involves the development of systems of manipulation that will be essential for the study of the molecular basis of any phenotypic property of F. nucleatum and possibly other related gram- negative anaerobic pathogens.
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