Identification of a gene at 16q24.3 that restores cellular senescence in immortal mammary tumor cells
Identification of a gene at 16q24.3 that restores cellular senescence in immortal mammary tumor cells
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DOI：
10.1038/sj.onc.1202888
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发表时间：
1999-09-09
期刊：
影响因子：
8
通讯作者：
Kaur, GP
中科院分区：
文献类型：
--
作者：
Reddy, DE;Sandhu, AK;Kaur, GP
我们已经定位了一个细胞衰老基因SEN16，在3-7 cM的遗传距离内，在16q24.3。微细胞介导的人类正常染色体16,16q22 -qter或16q23-qter的转移恢复了来自人和大鼠乳腺肿瘤的四种永生细胞系的细胞衰老。不确定细胞增殖的恢复，与供体染色体的分离一致，证实了在16q23-qter上存在衰老基因。当在选择培养基中保持微细胞杂交以保留供体染色体时，在衰老细胞中产生零星的不朽的可逆克隆。由于衰老基因的失活或突变或缺失，可以恢复到不朽的生长。对衰老微细胞杂交种的16号染色体特异性DNA标记的分析显示，在16q24.3位点存在一致性缺失，遗传间隔约为3-7 cM。
We have mapped a cellular senescence gene, SEN16, within a genetic distance of 3-7 cM, at 16q24.3. Microcell mediated transfer of a normal human chromosome 16, 16q22-qter or 16q23-qter restored cellular senescence in four immortal cell lines, derived from human and rat mammary tumors. The resumption of indefinite cell proliferation, concordant with the segregation of the donor chromosome, confirmed the presence of a senescence gene at 16q23-qter. While microcell hybrids were maintained in selection medium to retain the donor chromosome, sporadic immortal revertant clones arose among senescent cells. Reversion to immortal growth could occur due to inactivation of the senescence gene either by a mutation or a deletion. The analysis for chromosome 16 specific DNA markers, in revertant clones of senescent microcell hybrids, revealed a consensus deletion, spanning a genetic interval of approximately 3-7 cM at 16q24.3.