LINKAGE OF MANCHETTE MICROTUBULES TO THE NUCLEAR-ENVELOPE AND OBSERVATIONS OF THE ROLE OF THE MANCHETTE IN NUCLEAR SHAPING DURING SPERMIOGENESIS IN RODENTS
LINKAGE OF MANCHETTE MICROTUBULES TO THE NUCLEAR-ENVELOPE AND OBSERVATIONS OF THE ROLE OF THE MANCHETTE IN NUCLEAR SHAPING DURING SPERMIOGENESIS IN RODENTS
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DOI：
10.1002/aja.1001920202
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发表时间：
1991-10-01
影响因子：
--
通讯作者：
MEISTRICH, ML
中科院分区：
文献类型：
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作者：
RUSSELL, LD;RUSSELL, JA;MEISTRICH, ML
研究了小鼠和大鼠喉管的结构特征以及喉管在精子细胞核形成中的作用。在步骤8至步骤11中，可以看到直径约10纳米，长度约40-70纳米的棒状元件连接着最内层的微管和核膜的外层小叶，这些大鼠和小鼠精子要么是常规固定在电子显微镜下，要么是被分离并提取了洗涤剂。杆状连接物也可将核环连接到质膜和核膜上。这些连接可以确保在正常情况下，相对于这些膜性成分，manchette保持在一个确定的位置。各种化合物（紫杉醇、环磷酰胺和5-氟尿嘧啶）被发现扰乱了manchette并影响了核的形成。此外，sys和azh突变小鼠被用来确定颌骨形成缺陷的后果。这些遗传条件和化学处理要么产生不在其正常位置的manchette (azh、sys和taxol)，要么导致manchette出现异常（azh、sys、环磷酰胺、5-氟尿嘧啶和紫杉醇），所有这些都导致9-11步精子细胞核变形。在所有胸膜存在的情况下，无论是在正常位置还是异位位置，切片的核膜都平行于胸膜微管的长轴。一般来说，核膜中不存在胸膜的区域，或预期存在胸膜但没有的区域，呈圆形（正常动物，如环磷虾）。此外，有迹象表明，使用某些化合物（环磷酰胺和5-氟尿嘧啶）以及在azh和sys小鼠中，manchette可能施加压力使细胞核变形。这表明，在精子发生的早期伸长阶段，核包膜与核包膜微管保持恒定的距离，这是导致头部尾端至顶体区域核形状变化的主要因素。manchette微管，也被认为是连接在一起的，可能作为一个支架，使细胞核的这一部分从其球形变形，可能与其他结构元素引发的力相一致。来自5种动物的证据表明，结构因素，如顶体复合体（顶体-肌动蛋白-核包膜），可能影响精子头顶体覆盖部分的核形成。有人认为，染色质凝聚主要是加强了核幔层和其他作用于细胞核的结构元素已经带来的形状变化。染色质凝聚后，精细胞核形状变化不大。
Structural features of the mouse and rat manchette and the role of the manchette in shaping the spermatid nucleus were investigated. Rod-like elements about 10 nm in diameter and 40-70 nm in length were seen linking the innermost microtubules of the manchette and the outer leaflet of the nuclear envelope in step 8 through step 11 rat and mouse spermatids that either had been routinely fixed for electron microscopy or had been isolated and detergent extracted. Rod-like linkers were also seen joining the nuclear ring to the plasma membrane and nuclear envelope. These linkers may ensure that under normal conditions the manchette remains in a defined position relative to these membranous components. A variety of compounds (taxol, cytoxan, and 5-fluorouracil) were found to perturb the manchette and to affect nuclear shaping. In addition, sys and azh mutant mice were used to determine the consequences of defective manchette formation. These genetic conditions and chemical treatments either produced manchettes that were not in their normal position (azh, sys, and taxol) and/or caused the manchette to appear abnormal (azh, sys, cytoxan, 5-fluorouracil, and taxol), and all resulted in a deformation of the step 9-11 spermatid nucleus. In all instances where the manchette was present, either in normal or ectopic locations, the sectioned nuclear envelope was parallel to the long axis of the microtubules of the manchette. In general, areas of the nuclear envelope where the manchette was not present, or where it was expected to be present but was not, were rounded (normal animals, sys, cytoxan). In addition, there are indications using certain compounds (cytoxan and 5-fluorouracil) as well as in the azh and sys mouse that the manchette may exert pressure to deform the nucleus. It is suggested that the rod-like linkages of the manchette ensure that the nuclear envelope remains at a constant distance from the manchette microtubules and that this is a major factor acting to impart nuclear shape changes on a region of the head caudal to the acrosome during the early elongation phase of spermiogenesis. The manchette microtubules, which are also known to be linked together, may act as a scaffold to deform this part of the nucleus from its spherical shape, perhaps in concert with forces initiated by other structural elements. Evidence from sys animals indicates that structural elements, such as the acrosomal complex over the anterior head (acrosome-actin-nuclear envelope), may affect nuclear shaping over the acrosome-covered portion of the spermatid head. It is suggested that chromatin condensation primarily reinforces the shape changes already brought about by the manchette and other structural elements acting on the nucleus. After chromatin condensation, spermatid nuclear shape changes are minor.