Galandrini R, Henning S W, Cantrell D A
Lymphocyte Activation Laboratory, Imperial Cancer Research Fund Laboratories, London, United Kingdom.
Immunity. 1997 Jul;7(1):163-74. doi: 10.1016/s1074-7613(00)80519-1.
Mice lacking thymic function of the GTPase Rho show severe defects in fetal and adult thymopoiesis. Rho thymi are deficient in CD44+ CD25+ pro-T cells and CD44- CD25+ early pre-T cells because Rho function is required for survival but not G1/S phase cell cycle progression in these populations. The selective apoptosis defect in Rho prothymocytes can be rescued by expression of a bcl-2 transgene. A second function for Rho is seen in CD44- CD25- late pre-T cells: Rho regulates cell cycle progression but not survival of this population. These studies show that the critical processes of proliferation and survival are independently regulated during thymopoiesis and establish two different functions for Rho in the development of early thymic progenitors.
缺乏GTP酶Rho胸腺功能的小鼠在胎儿期和成年期的胸腺生成中表现出严重缺陷。Rho基因缺陷的胸腺中CD44+ CD25+ 前T细胞和CD44- CD25+ 早期前T细胞数量不足,因为这些细胞群体的存活需要Rho功能,但G1/S期细胞周期进程不需要。通过表达bcl-2转基因可以挽救Rho前胸腺细胞中的选择性凋亡缺陷。在CD44- CD25- 晚期前T细胞中发现了Rho的第二个功能:Rho调节该细胞群体的细胞周期进程,但不调节其存活。这些研究表明,在胸腺生成过程中,增殖和存活的关键过程是独立调节的,并确定了Rho在早期胸腺祖细胞发育中的两种不同功能。