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Hybrid breakdown and mitochondrial dysfunction in hybrids of Nasonia parasitoid wasps

机译:Nasonia寄生蜂杂交的杂种优势与线粒体功能障碍。

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摘要

Male F-2 hybrids of the wasps Nasonia giraulti and Nasonia vitripennis suffer increased mortality during development. Previous studies suggested that the mitochondria may play an important role in this pattern of hybrid breakdown. The mitochondrial genome encodes 13 polypeptides, which are integral subunits of the oxidative phosphorylation enzyme complexes I, III, IV and V. We show that the mitochondrial ATP production rate and the efficacy of the enzyme complexes I, III and IV, but not that of the completely nuclear-encoded complex II, are reduced in F-2 hybrid males of N. giraulti and N. vitripennis. We hypothesize that nuclear-mitochondrial protein interactions in the oxidative phosphorylation pathway are disrupted in these hybrids, reducing energy generation capacity and potentially reducing hybrid fitness. Our results suggest that dysfunctional cytonuclear interactions could represent an under-appreciated post-zygotic isolation mechanism that, due to elevated evolutionary rates of mitochondrial genes, evolves very early in the speciation process.
机译:黄蜂Nasonia giraulti和Nasonia vitripennis的雄性F-2杂种在发育过程中死亡率增加。先前的研究表明,线粒体可能在这种杂化分解模式中起重要作用。线粒体基因组编码13个多肽,它们是氧化磷酸化酶复合物I,III,IV和V的不可或缺的亚基。我们显示了线粒体ATP的产生速率和酶复合体I,III和IV的功效,但不包括G.aultiri和vitripennis的F-2杂种雄性中,完全核编码的复合物II减少。我们假设,在这些杂种中,氧化磷酸化途径中的核-线粒体蛋白质相互作用被破坏,从而降低了能量产生能力并潜在地降低了杂种适应性。我们的结果表明,功能失调的细胞核相互作用可能代表了一种未被充分认识的合子后分离机制,由于线粒体基因的进化速率提高,它在物种形成过程的早期就进化了。

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