Ye Xiaofen, Zerlanko Brad, Zhang Rugang, Somaiah Neeta, Lipinski Marc, Salomoni Paolo, Adams Peter D
Department of Basic Science, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA.
Mol Cell Biol. 2007 Apr;27(7):2452-65. doi: 10.1128/MCB.01592-06. Epub 2007 Jan 22.
Cellular senescence is an irreversible proliferation arrest triggered by short chromosome telomeres, activated oncogenes, and cell stress and mediated by the pRB and p53 tumor suppressor pathways. One of the earliest steps in the senescence program is translocation of a histone chaperone, HIRA, into promyelocytic leukemia (PML) nuclear bodies. This relocalization precedes other markers of senescence, including the appearance of specialized domains of facultative heterochromatin called senescence-associated heterochromatin foci (SAHF) and cell cycle exit. SAHF represses expression of proliferation-promoting genes, thereby driving exit from the cell cycle. HIRA bound to another histone chaperone, ASF1a, drives formation of SAHF. Here, we show that HIRA's translocation to PML bodies occurs in response to all senescence triggers tested. Dominant negative HIRA mutants that block HIRA's localization to PML bodies prevent formation of SAHF, as does a PML-RARalpha fusion protein which disrupts PML bodies, directly supporting the idea that localization of HIRA to PML bodies is required for formation of SAHF. Significantly, translocation of HIRA to PML bodies occurs in the absence of functional pRB and p53 tumor suppressor pathways. However, our evidence indicates that downstream of HIRA's localization to PML bodies, the HIRA/ASF1a pathway cooperates with pRB and p53 to make SAHF, with the HIRA/ASF1a and pRB pathways acting in parallel. We present evidence that convergence of the HIRA/ASF1a and pRB pathways occurs through a DNAJ-domain protein, DNAJA2.
细胞衰老指的是由短染色体端粒、激活的癌基因和细胞应激引发,并由pRB和p53肿瘤抑制途径介导的不可逆增殖停滞。衰老程序中最早的步骤之一是组蛋白伴侣HIRA易位至早幼粒细胞白血病(PML)核体。这种重新定位先于其他衰老标志物出现,包括称为衰老相关异染色质灶(SAHF)的兼性异染色质特殊结构域的出现以及细胞周期退出。SAHF抑制促进增殖基因的表达,从而促使细胞退出细胞周期。与另一种组蛋白伴侣ASF1a结合的HIRA驱动SAHF的形成。在此,我们表明,HIRA易位至PML体的现象在所有测试的衰老触发因素作用下均会发生。阻断HIRA定位至PML体的显性负性HIRA突变体可阻止SAHF的形成,破坏PML体的PML-RARα融合蛋白也有同样的作用,这直接支持了HIRA定位至PML体是SAHF形成所必需的这一观点。值得注意的是,在缺乏功能性pRB和p53肿瘤抑制途径的情况下,HIRA仍会易位至PML体。然而,我们的证据表明,在HIRA定位至PML体的下游,HIRA/ASF1a途径与pRB和p53协同作用以形成SAHF,其中HIRA/ASF1a和pRB途径并行发挥作用。我们提供的证据表明,HIRA/ASF1a和pRB途径通过一种DNAJ结构域蛋白DNAJA2发生汇聚。