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首页> 外文期刊>Molecular and Cellular Biology >Targeted Disruption of the Transition Protein 2 Gene Affects Sperm Chromatin Structure and Reduces Fertility in Mice
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Targeted Disruption of the Transition Protein 2 Gene Affects Sperm Chromatin Structure and Reduces Fertility in Mice

机译：靶向破坏过渡蛋白2基因影响精子染色质结构并降低小鼠的生育力。

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During mammalian spermiogenesis, major restructuring of chromatin takes place. In the mouse, the histones are replaced by the transition proteins, TP1 and TP2, which are in turn replaced by the protamines, P1 and P2. To investigate the role of TP2, we generated mice with a targeted deletion of its gene, Tnp2. Spermatogenesis inTnp2 null mice was almost normal, with testis weights and epididymal sperm counts being unaffected. The only abnormality in testicular histology was a slight increase of sperm retention in stage IX to XI tubules. Epididymal sperm from Tnp2-null mice showed an increase in abnormal tail, but not head, morphology. The mice were fertile but produced small litters. In step 12 to 16 spermatid nuclei from Tnp2-null mice, there was normal displacement of histones, a compensatory translationally regulated increase in TP1 levels, and elevated levels of precursor and partially processed forms of P2. Electron microscopy revealed abnormal focal condensations of chromatin in step 11 to 13 spermatids and progressive chromatin condensation in later spermatids, but condensation was still incomplete in epididymal sperm. Compared to that of the wild type, the sperm chromatin of these mutants was more accessible to intercalating dyes and more susceptible to acid denaturation, which is believed to indicate DNA strand breaks. We conclude that TP2 is not a critical factor for shaping of the sperm nucleus, histone displacement, initiation of chromatin condensation, binding of protamines to DNA, or fertility but that it is necessary for maintaining the normal processing of P2 and, consequently, the completion of chromatin condensation.
机译：在哺乳动物的精子发生过程中，染色质发生了重大的重组。在小鼠中，组蛋白被过渡蛋白TP1和TP2取代，而过渡蛋白又被鱼精蛋白P1和P2取代。为了研究TP2的作用，我们产生了有针对性地删除其基因 Tnp2 的小鼠。在 Tnp2 无效小鼠中，精子生成几乎是正常的，睾丸重量和附睾精子计数不受影响。睾丸组织学中唯一的异常是第IX至XI期小管的精子保留量略有增加。 Tnp2 -空小鼠的附睾精子异常尾巴增加，但头部形态没有增加。小鼠可育，但产仔少。在 Tnp2 -null小鼠的第12至16步精子细胞核中，组蛋白正常移位，TP1水平通过补偿性翻译调节增加，P2的前体和部分加工形式水平升高。电子显微镜显示，在第11至13步精子中染色质出现异常的局部凝集，而在后来的精子中，染色质逐渐进行凝结，但附睾精子中的凝结仍不完全。与野生型相比，这些突变体的精子染色质更易于嵌入染料，并且更容易发生酸变性，据信这表明DNA链断裂。我们得出结论，TP2不是精子核的形状，组蛋白置换，染色质凝结的起始，鱼精蛋白与DNA的结合或受精的关键因素，但对于维持P2的正常加工并因此完成染色质凝聚。

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