MECHANISM OF CHLAMYDIA-INDUCED CENTROSOME AMPLIFICATION

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 在流行病学研究中，沙眼衣原体是细菌性传播感染的最常见原因，与宫颈癌有关。这种联系可能涉及衣原体感染对中心体的影响，其特征是中心体复制失调和出现多个中心体病灶。然而，这些中心体异常还没有在超微结构水平上进行分析。我们发现，中心体调节因子HsSAS-6在衣原体感染期间被蛋白水解性修饰。HsSAS-6被切割，产生足以引起中心体扩增的稳定切割产物。我们的目标是在超微结构水平上确定对HsSAS-6的蛋白降解作用是否足以导致衣原体感染细胞的中心体扩增表型。

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.