鼠标X链微RNA集群以拷贝数依赖的方式调节介质检查点和Prdm9驱动的杂交不育
Petr Jansa1,2, Giordano Tanieli1,2, Kim Vucinic1,3
1Laboratory of Mouse Molecular Genetics, Institute of Molecular Genetics, Czech Academy of Sciences, Praha 142 20, Czech Republic.
概括
微RNA 465 (MIR465) 基因集群通过与PRDM9相互作用,解决了小鼠中的混合雄性不孕症. 删除MIR465基因可以恢复生育能力并改善半分裂,从而提供了对物种化和多布尚斯基-穆勒不相容性的见解.
科学领域:
- 进化遗传学 进化遗传学
- 生殖生物学 生殖生物学
- 分子遗传学 分子遗传学
背景情况:
- 杂交不育是新物种形成期间的一个关键的繁殖障碍.
- 在Mus musculus musculus × Mus musculus domesticus杂交物种中观察到的不孕不育是由PRDM9和一个未知的X相关因子 (杂交不孕不育X2,Hstx2) 驱动的.
研究的目的:
- 为了确定在Hstx2位点对混合男性不孕症负责的遗传因素.
- 调查这种因素在杂交生育,半变和重组中的作用.
主要方法:
- 基因分析以确定Hstx2因子.
- 在小鼠中的Mir465微RNA (miRNA) 集群的基因淘汰.
- 评估混合生育,介质突触和精子生成.
- 全球重组率的测量.
主要成果:
- 标识了Mir465 miRNA基因集群作为Hstx2杂交不孕症因子.
- 删除Mir465基因恢复了生育能力,并改善了无菌杂交动物中的中介突触.
- Mir465淘汰赛还在染色体转移载体中拯救了精子生成,作为一个介质检查点.
- 米尔465淘汰赛增加了混合体和Mus m. domesticus小鼠的全球重组率.
结论:
- Mir465负责混合不育 (Hstx2) 并影响重组率 (Meir1).
- PRDM9和Mir465之间的相互作用代表了Dobzhansky-Muller不兼容性.
- 在Mir465基因中的副本数变异可能会导致Mus m. musculus和Mus m. domesticus之间的生殖障碍.
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