Nguyen Hao G, Yu Guangyao, Makitalo Maria, Yang Dan, Xie Hou-Xiang, Jones Matthew R, Ravid Katya
Boston University School of Medicine, Department of Biochemistry, 715 Albany St, K225, Boston, MA 02118, USA.
Blood. 2005 Sep 1;106(5):1559-64. doi: 10.1182/blood-2005-02-0638. Epub 2005 May 12.
Megakaryocyte (MK)-specific transgene expression has proved valuable in studying thrombotic and hemostatic processes. Constitutive expression of genes, however, could result in altered phenotypes due to compensatory mechanisms or lethality. To circumvent these limitations, we used the tetracycline/doxycycline (Tet)-off system to conditionally over-express genes in megakaryocytes and platelets in vivo. We generated 3 transactivator transgenic lines expressing the Tet transactivator element (tTA), under the control of the MK-specific platelet factor 4 promoter (PF4-tTA-VP16). Responder lines were simultaneously generated, each with a bidirectional minimal cytomegalovirus (CMV)-tTA responsive promoter driving prokaryotic beta-galactosidase gene, as a cellular reporter, and a gene of interest (in this case, the mitotic regulator Aurora-B). A transactivator founder line that strongly expressed PF4-driven tTA-viral protein 16 (VP16) was crossbred to a responder line. The homozygous double-transgenic mouse line exhibited doxycycline-dependent transgene overexpression in MKs and platelets. Using this line, platelets were conveniently indicated at sites of induced stress by beta-galactosidase staining. In addition, we confirmed our earlier report on effects of constitutive expression of Aurora-B, indicating a tight regulation at protein level and a modest effect on MK ploidy. Hence, we generated a new line, PF4-tTA-VP16, that is available for conditionally overexpressing genes of interest in the MK/platelet lineage in vivo.
巨核细胞(MK)特异性转基因表达已被证明在研究血栓形成和止血过程中具有重要价值。然而,由于补偿机制或致死性,基因的组成型表达可能导致表型改变。为了规避这些限制,我们使用四环素/强力霉素(Tet)诱导系统在体内条件性地在巨核细胞和血小板中过表达基因。我们构建了3个表达Tet反式激活元件(tTA)的反式激活转基因品系,其受MK特异性血小板因子4启动子(PF4-tTA-VP16)的控制。同时构建了响应品系,每个品系都有一个双向最小巨细胞病毒(CMV)-tTA响应启动子,驱动原核β-半乳糖苷酶基因作为细胞报告基因,以及一个目的基因(在本研究中为有丝分裂调节因子Aurora-B)。将一个强烈表达PF4驱动的tTA-病毒蛋白16(VP16)的反式激活转基因奠基品系与一个响应品系进行杂交。纯合双转基因小鼠品系在MK和血小板中表现出强力霉素依赖性转基因过表达。利用该品系,通过β-半乳糖苷酶染色可方便地在诱导应激部位指示血小板。此外,我们证实了我们之前关于Aurora-B组成型表达影响的报道,表明在蛋白质水平上有严格的调控,并且对MK倍性有适度的影响。因此,我们构建了一个新的品系PF4-tTA-VP16,可用于在体内条件性地过表达MK/血小板谱系中的目的基因。