DEFICIENCY OF X-CHROMOSOMAL AND Y-CHROMOSOMAL PAIRING AT MEIOTIC PROPHASE IN SPERMATOCYTES OF STERILE INTERSPECIFIC HYBRIDS BETWEEN LABORATORY MICE (MUS-DOMESTICUS) AND MUS-SPRETUS

DEFICIENCY OF X-CHROMOSOMAL AND Y-CHROMOSOMAL PAIRING AT MEIOTIC PROPHASE IN SPERMATOCYTES OF STERILE INTERSPECIFIC HYBRIDS BETWEEN LABORATORY MICE (MUS-DOMESTICUS) AND MUS-SPRETUS
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DOI:
10.1007/bf00352471
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发表时间:
1992-06-01
期刊:
影响因子:
1.6
通讯作者:
CHAPMAN, VM
CHAPMAN, VM
中科院分区:
生物学3区
文献类型:
--
作者:
MATSUDA, Y;MOENS, PB;CHAPMAN, VM

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在小鼠精母细胞的风干光学显微镜制备物中所见的减数分裂中期I的X和Y染色体之间的正常关联,在实验室小鼠品系C57 BL/6和Mus spretus之间的不育种间杂种的精母细胞中经常缺乏。 这项工作的目的是确定在杂种中分离的X和Y染色体是不联会的,由配对失败引起的,还是去联会的,由早熟分离引起的。 在终变期,即中期I之前,在风干的标本中观察到不配对的X-Y染色体。 此外,免疫细胞学和电子显微镜研究的表面蔓延粗线期精母细胞表明,X和Y染色体经常无法启动突触的判断失败,形成联会复合体之间的配对区域的X和Y染色体。 在杂种中观察到几个额外的染色体异常。 这些包括未配对的X或Y核心的折返,常染色体和性染色体核心之间的关联,以及常染色体单价体。 异常常染色体和XY-常染色体联合的发生也与减数分裂前期的细胞变性有关。 杂种精子发生的初级破坏发生在中期I(MI),MI晚期出现退化细胞。 在这些细胞中,X和Y是去致密化的,而不是像正常小鼠MI精母细胞中那样浓缩的。 结合前人对杂种和与可育雌性杂种回交后代精子发生的遗传分析,这些结果表明,种间杂种精子发生的破坏主要与减数分裂前期XY配对的失败、不联会以及中期I精母细胞的退化有关。 其次,XY配对的失败可能伴随着常染色体配对的失败,这似乎涉及异常的性囊泡和变性在粗线期或双线期。
The normal association between the X and Y chromosomes at metaphase I of meiosis, as seen in air-dried light microscope preparations of mouse spermatocytes, is frequently lacking in the spermatocytes of the sterile interspecific hybrid between the laboratory mouse strains C57BL/6 and Mus spretus. The purpose of this work is to determine whether the separate X and Y chromosomes in the hybrid are asynaptic, caused by failure to pair, or desynaptic, caused by precocious dissociation. Unpaired X-Y chromosomes were observed in air-dried preparations at diakinesis, just prior to metaphase I. Furthermore, immunocytology and electron microscopy studies of surface-spread pachytene spermatocytes indicate that the X and Y chromosomes frequently fail to initiate synapsis as judged by the failure to form a synaptonemal complex between the pairing regions of the X and Y chromosomes. Several additional chromosomal abnormalities were observed in the hybrid. These include fold-backs of the unpaired X or Y cores, associations between the autosome and sex chromosome cores, and autosomal univalents. The occurrence of abnormal autosomal and XY-autosomal associations was also correlated with cell degeneration during meiotic prophase. The primary breakdown in hybrid spermatogenesis occurs at metaphase I (MI), with the appearance of degenerated cells at late MI. In those cells, the X and Y are decondensed rather than condensed as they are in normal mouse MI spermatocytes. These results, in combination with the previous genetic analysis of spermatogenesis in hybrids and backcrosses with fertile female hybrids, suggest that the spermatogenic breakdown in the interspecific hybrid is primarily correlated with the failure of XY pairing at meiotic prophase, asynapsis, followed by the degeneration of spermatocytes at metaphase I. Secondarily, the failure of XY pairing can be accompanied by failure of autosomal pairing, which appears to involve an abnormal sex vesicle and degeneration at pachytene or diplotene.