Milbradt Jens, Auerochs Sabrina, Marschall Manfred
Virological Institute of the University Hospital Erlangen, Clinical and Molecular Virology, University of Erlangen-Nuremberg, 91054 Erlangen, Germany.
J Gen Virol. 2007 Oct;88(Pt 10):2642-2650. doi: 10.1099/vir.0.82924-0.
Human cytomegalovirus-encoded pUL50 and pUL53 belong to a group of conserved herpesviral nuclear proteins. This study describes: (i) the co-localization of pUL50 with components of the nuclear lamina such as lamins A/C and lamin B receptor by double immunofluorescent staining, (ii) a strong pUL50-mediated relocalization of pUL53 from a diffuse nuclear pattern towards a nuclear rim localization, (iii) a direct interaction between pUL50 and pUL53, as well as between pUL50 and protein kinase C (PKC), shown by yeast two-hybrid and co-immunoprecipitation analyses, (iv) in vitro phosphorylation of pUL50, which is highly suggestive of PKC activity, and finally (v) partial relocalization of PKC by pUL50/pUL53 from its main cytoplasmic localization to a marked nuclear lamina accumulation. These data suggest a role for pUL50 and pUL53 in the recruitment of PKC, an event that is considered to be important for cytomegalovirus-induced distortion of the nuclear lamina.
人巨细胞病毒编码的pUL50和pUL53属于一组保守的疱疹病毒核蛋白。本研究描述了:(i) 通过双重免疫荧光染色,pUL50与核纤层成分如核纤层蛋白A/C和核纤层蛋白B受体的共定位;(ii) pUL50介导的pUL53从弥漫性核模式向核边缘定位的强烈重新定位;(iii) 酵母双杂交和共免疫沉淀分析显示pUL50与pUL53之间以及pUL50与蛋白激酶C (PKC) 之间的直接相互作用;(iv) pUL50的体外磷酸化,这强烈提示PKC活性;最后(v) pUL50/pUL53使PKC从其主要的细胞质定位部分重新定位到明显的核纤层积累处。这些数据表明pUL50和pUL53在PKC募集过程中发挥作用,这一事件被认为对巨细胞病毒诱导的核纤层变形很重要。