Russell L D, Ying L, Overbeek P A
Department of Physiology, Southern Illinois University, School of Medicine, Carbondale 62901-6512.
Anat Rec. 1994 Apr;238(4):437-53. doi: 10.1002/ar.1092380403.
A family of transgenic mice (OVE 219) was generated by microinjection of a tyrosinase minigene (Ty811C). The transgenic mice demonstrate an atypical and variable coat color pattern and the homozygous males show abnormalities of spermatogenesis that are variably expressed from animal to animal. Heterozygous mice proved to have normal spermatogenesis and along with non-transgenic mice were used as controls to study the abnormalities in spermatogenesis in OVE 219 homozygous males. These abnormalities shed light on the features controlling normal spermatogenesis. In some homozygous males early spermiogenesis was disrupted as the flagellar microtubules became disorganized within the flagellar process. What appeared to be crystalline tubulin was noted within some of the rounded flagellar processes. Sperm with this defect did not develop a flagellum. In other homozygous males defects were apparent by step 6 or 7 of spermiogenesis when the acrosome did not grow and spread over the nucleus as noted in control animals. The modified nuclear envelope underlying the acrosome continued to develop and spread well beyond one margin of the acrosome. Since the modified nuclear envelope grew independently of the acrosome, the acrosome was not the controlling factor in determining the spread of the modified nuclear envelope. Micrographs revealed that Sertoli ectoplasmic specialization failed to form over most regions of the spermatid head lacking a normal acrosome. In homozygous males, the manchette took origin (proximally) in close relation to the modified nuclear envelope and never in relation to the edge of the spreading acrosome, a feature indicating that manchette placement was influenced by the position of the modified nuclear envelope and not the edge of the acrosome. Thus the modification in the nuclear envelope may be the primary event to signal acrosomal spread and manchette development. In spermatids where the manchette developed from an ectopic site, the result was abnormal caudal head shaping. In some spermatids a portion of the manchette was lacking. When this occurred the caudal head was rounded in the region of the missing manchette. In a minority of spermatids there was no evidence for a manchette. The entire caudal head was gently rounded. These data support the growing body of evidence that the caudal sperm head is shaped, in part, by the manchette. The OVE 219 family of mice provides a useful model to understand the processes involved in periods of spermiogenesis that are critical to development of a normally shaped sperm head.
通过显微注射酪氨酸酶小基因（Ty811C）构建了一个转基因小鼠家族（OVE 219）。这些转基因小鼠表现出非典型且多变的毛色模式，纯合子雄性小鼠表现出精子发生异常，且不同动物之间的异常表现存在差异。杂合子小鼠的精子发生被证明是正常的，它们与非转基因小鼠一起被用作对照，以研究OVE 219纯合子雄性小鼠的精子发生异常情况。这些异常情况为控制正常精子发生的特征提供了线索。在一些纯合子雄性小鼠中，早期精子形成过程受到破坏，因为鞭毛微管在鞭毛形成过程中变得紊乱。在一些圆形的鞭毛形成过程中发现了似乎是结晶微管蛋白的物质。有这种缺陷的精子没有发育出鞭毛。在其他纯合子雄性小鼠中，精子形成的第6或第7步出现明显缺陷，此时顶体不像对照动物那样生长并覆盖细胞核。顶体下方的修饰核膜继续发育并扩展到顶体的一侧边缘之外。由于修饰核膜独立于顶体生长，顶体不是决定修饰核膜扩展的控制因素。显微照片显示，在缺乏正常顶体的精子细胞头部的大部分区域，支持细胞的胞质特化未能形成。在纯合子雄性小鼠中，袖套（manchette）起源于（近端）与修饰核膜密切相关的位置，而从不与扩展顶体的边缘相关，这一特征表明袖套的位置受修饰核膜位置的影响，而不是顶体边缘的影响。因此，核膜的修饰可能是信号顶体扩展和袖套发育的主要事件。在袖套从异位部位发育的精子细胞中，结果是尾部头部形状异常。在一些精子细胞中，袖套的一部分缺失。当这种情况发生时，尾部头部在缺失袖套的区域呈圆形。在少数精子细胞中，没有袖套的证据。整个尾部头部呈柔和的圆形。这些数据支持了越来越多的证据表明，精子尾部头部的形状部分是由袖套塑造的。OVE 219小鼠家族为理解精子形成过程中对正常形状精子头部发育至关重要的阶段所涉及的过程提供了一个有用的模型。
