MECHANISM OF CHLAMYDIA-INDUCED CENTROSOME AMPLIFICATION

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 沙眼衣原体是细菌性性传播感染的最常见原因，在流行病学研究中与宫颈癌有关。这种关联可能涉及衣原体感染对中心体的影响，其特征在于中心体复制失调和多个中心体病灶的出现。然而，这些中心体异常尚未在超微结构水平上进行分析。我们已经发现，中心体调节HsSAS-6是蛋白水解修改衣原体感染期间。HsSAS-6被切割，产生足以引起中心体扩增的稳定切割产物。这是我们的目标，以确定在超微结构水平上是否对HsSAS-6蛋白水解作用足以导致扩增的衣原体感染的细胞的中心体表型。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Chlamydia trachomatis, the most common cause of bacterial sexually transmitted infection, has been linked to cervical cancer in epidemiologic studies. This association may involve effects of a chlamydial infection on the centrosome that are characterized by dysregulation of centrosome duplication and appearance of multiple centrosomal foci. However, these centrosome abnormalities have not been analyzed at an ultrastructural level. We have found that the centrosomal regulator HsSAS-6 is proteolytically modified during a chlamydial infection. HsSAS-6 is cleaved, producing stable cleavage products that are sufficient to cause centrosome amplification. It is our goal to determine on an ultrastructural level whether proteolytic effects on HsSAS-6 are sufficient to cause the amplified centrosome phenotype of Chlamydia-infected cells.