水稻基因组结构变异介导的等位基因表达抑制及其杂种不育

来源 :2016全国植物生物学大会 | 被引量 : 0次 | 上传用户:nihaoyuyue2009
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  杂种不育是种间或亚种间的生殖隔离机制。籼稻和粳稻亚种间杂种具有很强的杂种优势,但严重的杂种不育妨碍了籼粳杂种产量潜力的利用。籼粳杂种不育由多个座位控制。我们以前克隆的Sa座位由2个相邻的等位分化基因间互作控制籼粳杂种雄性不育。我们利用图位克隆分离了一个新座位Sc的籼粳等位基因。粳稻等位基因Sc-j编码一个花粉配子体发育必需的DUF1618蛋白。测序分析发现,籼稻等位基因Sc-i发生了很大的结构变异:与Sc-j基因对应的基因有2个转座子插入成为假基因,而该假基因下游有2个或3个28kb片段顺向重复(不同籼稻品种拷贝数不同),每个重复含有一个Sc-j同源基因,但它们的启动子及其上游区序列与Sc-j的启动子序列完全不同。在Sc杂合体(杂种F1),Sc-i表达产物介导了对Sc-j的表达抑制而导致Sc-j花粉的败育。含有3个Sc-i拷贝的籼粳杂种比含有2个Sc-i拷贝的产生更严重的杂种不育。我们在杂种以CRISPR/Cas9敲除或突变1-2个Sc-i拷贝,降低Sc-i基因剂量和表达水平,结果可以提升Sc-j表达并恢复花粉育性。我们提出了一种Sc等位互作控制杂种不育的分子遗传模型。本研究表明基因组结构和拷贝数变异是基因组进化和遗传性状变异的重要机制,揭示了Sc座位的分子遗传基础,还建立了利用基因编辑创建杂种亲和等位基因以利用杂种优势的技术方法。
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