Dyban A P, Noniashvili E M, Freĭdin M I
Institute of Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg, Russia.
Ontogenez. 1998 Mar-Apr;29(2):113-22.
We carried out a cytogenetic study of ovulating oocytes and unicellular embryos, heterozygous by reciprocal chromosomal translocation T[14;15]6Ca. Okadaic acid was used to induce premature condensation of the interphase chromosomes in the embryos, and the number of G1 chromosomes was counted in the second polar body and pronuclei. It was shown that cytogenetic analysis of the sister chromosomal sets adequately determines the frequency of chromosomal segregation errors during oocyte meioses I and II. Trisomy and monosomy were observed in 36.2% embryos, while 2.2% featured tetrasomy or double monosomy. Errors of the first meiotic division caused aneuploidy in 28.5% embryos; trisomy and monosomy resulted from the homologs non-disjunction and chromatid presegregation in 17.6 and 10.9%, respectively. Numeral chromosomal aberrations in 4.1% of the embryos resulted from abnormal chromosomal segregation during oocyte meiosis II, while paternal chromosomal aberrations were found in 5.8% embryos. The main advantage of the proposed method is not only the higher accuracy in estimating the meiotic error frequency, but also the possibility to trace the origin of aneuploidy in mammalian embryos.
我们对排卵的卵母细胞和单细胞胚胎进行了细胞遗传学研究,这些细胞因相互染色体易位T[14;15]6Ca而呈杂合状态。使用冈田酸诱导胚胎中期染色体过早凝聚,并在第二极体和原核中计数G1期染色体的数量。结果表明,对姐妹染色体组进行细胞遗传学分析能够充分确定卵母细胞减数分裂I和II期间染色体分离错误的频率。在36.2%的胚胎中观察到三体性和单体性,而2.2%的胚胎表现为四体性或双单体性。第一次减数分裂错误在28.5%的胚胎中导致非整倍性;三体性和单体性分别由同源染色体不分离和染色单体预分离导致,比例分别为17.6%和10.9%。4.1%的胚胎中数字染色体畸变是由卵母细胞减数分裂II期间染色体异常分离导致的,而5.8%的胚胎中发现了父本染色体畸变。所提出方法的主要优点不仅在于估计减数分裂错误频率时具有更高的准确性,还在于能够追踪哺乳动物胚胎中非整倍性的起源。