Ruthardt M, Orleth A, Tomassoni L, Puccetti E, Riganelli D, Alcalay M, Mannucci R, Nicoletti I, Grignani F, Fagioli M, Pelicci P G
European Institute of Oncology, Department of Experimental Oncology, Milan, Italy.
Oncogene. 1998 Apr 16;16(15):1945-53. doi: 10.1038/sj.onc.1201722.
Acute promyelocytic leukaemia is characterized by translocations that involve the retinoic acid receptor alpha (RAR alpha) locus on chromosome 17 and the PML locus on 15 or the PLZF locus on 11. The resulting abnormal translocation products encode for PML/RAR alpha or PLZF/RAR alpha fusion proteins. There is increasing experimental evidence that the APL-specific fusion proteins have similar biologic activities on differentiation and survival and that both components of the fusion proteins (PML or PLZF and RAR alpha) are indispensable for these biological activities. The physiologic function of PML or PLZF or whether PML and PLZF contribute common structural or functional features to the corresponding fusion proteins is not known. We report here immunofluorescence studies on the cellular localization of PLZF and PLZF/RAR alpha and compare it with the localization of PML and PML/RAR alpha. PLZF localizes to nuclear domains of 0.3-0.5 microns, approximately 14 per cell in the KG1 myeloid cell line. These PLZF-bodies are morphologically similar to the domains reported for PML (PML-NBs). There is tight spatial relationship between about 30% of PLZ-NBs and PML-NBs: they partially overlap. However, PML and PLZF do not form soluble complexes in vivo. PLZF- and PML-NBs are functionally distinct. Adenovirus E4-ORF3 protein expression alters the structure of the PML-NBs and interferon increases the number of PML-NBs and neither has any effect on PLZF NBs. The localization of PLZF/RAR alpha is different to that of PLZF and RAR alpha. The nuclear distribution pattern of PLZF/RAR alpha is one of hundreds of small dots (microspeckles) less than 0.1 micron. Expression of PLZF/RAR alpha did not provoke disruption of the PML-NBs. Co-expression of PML/RAR alpha and PLZF/RAR alpha in U937 cells revealed apparent colocalization. Overall the results suggest that the PML- and PLZF-NBs are distinct functional nuclear domains, but that they may share common regulatory pathways and/or targeting sequences, as revealed by the common localization of their corresponding fusion proteins.
急性早幼粒细胞白血病的特征是涉及17号染色体上的维甲酸受体α(RARα)基因座与15号染色体上的PML基因座或11号染色体上的PLZF基因座的易位。产生的异常易位产物编码PML/RARα或PLZF/RARα融合蛋白。越来越多的实验证据表明,APL特异性融合蛋白在分化和存活方面具有相似的生物学活性,并且融合蛋白的两个组分(PML或PLZF和RARα)对于这些生物学活性都是不可或缺的。PML或PLZF的生理功能,或者PML和PLZF是否对相应的融合蛋白具有共同的结构或功能特征尚不清楚。我们在此报告关于PLZF和PLZF/RARα细胞定位的免疫荧光研究,并将其与PML和PML/RARα的定位进行比较。在KG1髓系细胞系中,PLZF定位于0.3 - 0.5微米的核结构域,每个细胞约有14个。这些PLZF小体在形态上与报道的PML结构域(PML-NBs)相似。约30%的PLZ-NB与PML-NB之间存在紧密的空间关系:它们部分重叠。然而,PML和PLZF在体内不形成可溶性复合物。PLZF-和PML-NB在功能上是不同的。腺病毒E4-ORF3蛋白表达改变PML-NB的结构,干扰素增加PML-NB的数量,而两者对PLZF小体均无任何影响。PLZF/RARα的定位与PLZF和RARα不同。PLZF/RARα的核分布模式是数百个小于0.1微米的小点(微斑点)之一。PLZF/RARα的表达未引起PML-NB的破坏。PML/RARα和PLZF/RARα在U937细胞中的共表达显示出明显的共定位。总体而言,结果表明PML-和PLZF-NB是不同的功能性核结构域,但正如它们相应融合蛋白的共同定位所揭示的那样,它们可能共享共同的调节途径和/或靶向序列。