Matsuda Y, Moens P B, Chapman V M
Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, NY 14263.
Chromosoma. 1992 Jun;101(8):483-92. doi: 10.1007/BF00352471.
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.
在小鼠精母细胞的空气干燥光镜标本中可以看到，减数分裂中期I时X和Y染色体之间的正常配对，在实验室小鼠品系C57BL/6和西班牙小鼠（Mus spretus）的不育种间杂种的精母细胞中常常缺失。这项工作的目的是确定杂种中分离的X和Y染色体是由于未能配对而导致的不联会，还是由于过早解离而导致的解联会。在终变期（紧接中期I之前）的空气干燥标本中观察到未配对的X-Y染色体。此外，对表面铺展的粗线期精母细胞的免疫细胞学和电子显微镜研究表明，根据X和Y染色体配对区域之间未能形成联会复合体判断，X和Y染色体常常未能启动联会。在杂种中还观察到其他几种染色体异常。这些异常包括未配对的X或Y核心的折返、常染色体核心与性染色体核心之间的关联以及常染色体单价体。常染色体和XY-常染色体异常关联的发生也与减数分裂前期的细胞退化相关。杂种精子发生的主要故障发生在中期I（MI），在MI后期出现退化细胞。在那些细胞中，X和Y是解聚的，而不是像正常小鼠MI精母细胞那样凝聚。这些结果，结合先前对杂种精子发生以及与可育雌性杂种回交的遗传分析，表明种间杂种中精子发生故障主要与减数分裂前期XY配对失败、不联会相关，随后是中期I精母细胞的退化。其次，XY配对失败可能伴随着常染色体配对失败，这似乎涉及异常的性泡以及粗线期或双线期的退化。
