遗传 ›› 2021, Vol. 43 ›› Issue (12): 1121-1131.doi: 10.16288/j.yczz.21-205
袁露1,2(), 葛婷婷1,2, 牛长敏1,2, 徐文华1,2, 郑英1,2()
收稿日期:
2021-06-10
修回日期:
2021-10-27
出版日期:
2021-12-20
发布日期:
2021-11-10
通讯作者:
郑英
E-mail:2920054914@qq.com;yzzkl@163.com
作者简介:
袁露,在读硕士研究生,专业方向:生殖医学。E-mail: 基金资助:
Lu Yuan1,2(), Tingting Ge1,2, Changmin Niu1,2, Wenhua Xu1,2, Ying Zheng1,2()
Received:
2021-06-10
Revised:
2021-10-27
Online:
2021-12-20
Published:
2021-11-10
Contact:
Zheng Ying
E-mail:2920054914@qq.com;yzzkl@163.com
Supported by:
摘要:
精子形成是精子发生的最后阶段,圆形精子细胞经历了一系列的形态变化和染色质凝聚,形成了具有物种特异性的成熟精子。组蛋白-鱼精蛋白替换是精子形成过程中的重要事件。在组蛋白-鱼精蛋白替换过程中,组蛋白首先被睾丸特异性的组蛋白变体所替代,随后过渡蛋白整合到细胞核中,最后过渡蛋白被鱼精蛋白取代。组蛋白-鱼精蛋白替换缺陷可能导致无精子症、少精子症或畸精症,从而导致男性不育。本文系统总结了组蛋白-鱼精蛋白替换过程中的调控机制研究进展,以期为男性不育症的诊断和治疗提供理论基础。
袁露, 葛婷婷, 牛长敏, 徐文华, 郑英. 精子变形过程中组蛋白-鱼精蛋白替换调控机制[J]. 遗传, 2021, 43(12): 1121-1131.
Lu Yuan, Tingting Ge, Changmin Niu, Wenhua Xu, Ying Zheng. Regulation of histone-to-protamine transition during spermiogenesis[J]. Hereditas(Beijing), 2021, 43(12): 1121-1131.
表1
组蛋白-鱼精蛋白替换调控相关基因"
基因 | 基因敲除表型 | 功能 | 参考文献 |
---|---|---|---|
H1t | 雄性生育力正常 | 诱导局部染色质松弛 | [ |
H1t2 | 雄性不育 | 参与PRM的掺入与染色质凝聚 | [ |
Th2a/Th2b | 雄性不育 | 调节染色质开放或总组蛋白水平 | [ |
H2al2 | 雄性不育 | 组装开放的核小体并允许TP掺入 | [ |
H2a.b | 雄性生育力下降 | 调节H2AL2的解聚和TP1的掺入 | [ |
H3f3a/H3f3b | 雄性不育 | 有助于形成开放的染色质构型 | [ |
H3t | 雄性不育 | - | [ |
Epc1 | 雄性不育 | 参与组蛋白的超乙酰化 | [ |
Tip60 | 雄性不育 | 参与组蛋白的超乙酰化 | [ |
Brdt | 雄性不育 | 介导乙酰化组蛋白的替换 | [ |
Rnf8 | 雄性不育 | 单泛素化H2A和H2B,调节组蛋白的解聚 | [ |
Miwi | 雄性不育 | 对RNF8的核转位必不可少,并促进组蛋白泛素化和解聚 | [ |
L3mbtl2 | 雄性生育力下降 | 参与PRM1的沉积和染色质凝聚 | [ |
Phf7 | 雄性不育 | 识别H3K4me2/me3并催化H2A泛素化以促进组蛋白的解聚 | [ |
Pa200 | 雄性生育力下降 | 通过蛋白酶体介导乙酰化的组蛋白降解 | [ |
Tnp1/Tnp2 | 雄性生育力下降 | PRM2的掺入和染色质凝聚所必需 | [ |
Dazl | 雄性不育 | 调节TP mRNA的表达 | [ |
Jmjd1a | 雄性不育 | 调节精子基因组包装和染色质凝聚 | [ |
Prm1/Prm2 | 雄性不育 | 染色质凝聚所必需 | [ |
Camk4 | 雄性不育 | 介导PRM2磷酸化 | [ |
Ppp1cc2 | 雄性不育 | 使鱼精蛋白2第56位丝氨酸(Prm2Ser56)去磷酸化 | [ |
Ip6k1 | 雄性不育 | 调控TP2和PRM2的表达 | [ |
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