Verp M S, Rosinsky B, Le Beau M M, Martin A O, Kaplan R, Wallemark C B, Otano L, Simpson J L
Department of Obstetrics and Gynecology, University of Chicago, Illinois.
Clin Genet. 1988 Apr;33(4):277-85. doi: 10.1111/j.1399-0004.1988.tb03449.x.
We have previously shown that cell generation time (CGT) is prolonged in 45,X and certain X-deletion fibroblast lines (Simpson & Le Beau 1981). A consequence of that finding should be that cells with 45,X or an X-structural abnormality are at a competitive disadvantage when cocultivated with 46,XX cells. To test this hypothesis we prepared 15 minutes of cells from combinations of 9 different cell lines: four 45,X; one 46,Xdel(X)(p11); and four 46,XX. Each culture was monitored cytogenetically at frequent passage intervals for the percentage of the two cell lines. Significant differences were found between normal and abnormal lines in culture predominance, in the order predicted by our hypothesis (p less than 0.01). The specific mechanism by which absence of an X chromosome confers growth disadvantage is unknown, but is consistent with prolongation of CGT. Prolongation of CGT could also be responsible for the embryonic lethality, intrauterine growth retardation, short stature, and somatic anomalies commonly observed in individuals with absent or aberrant X chromosomes.
我们之前已经表明，在45,X及某些X缺失的成纤维细胞系中细胞生成时间（CGT）会延长（辛普森和勒博，1981年）。该发现的一个结果应该是，45,X或具有X结构异常的细胞在与46,XX细胞共培养时处于竞争劣势。为了验证这一假设，我们从9种不同细胞系的组合中制备了15分钟的细胞：4种45,X；1种46,Xdel(X)(p11)；以及4种46,XX。在频繁传代间隔时对每种培养物进行细胞遗传学监测，以观察两种细胞系的百分比。在培养优势方面，正常和异常细胞系之间发现了显著差异，其顺序符合我们假设所预测的（p小于0.01）。X染色体缺失导致生长劣势的具体机制尚不清楚，但与CGT延长一致。CGT延长也可能是X染色体缺失或异常个体中常见的胚胎致死、宫内生长迟缓、身材矮小和躯体异常的原因。
