内共生起源之后，细胞器基因组进化的最显著特征是：大量基因转移到细胞核中。理论上，基因转移有三个主要参与者：供体（细胞器基因组）、被转移者（DNA片段）和受体（核基因组）。深入调查文献发现，之前研究主要关注供体和被转移者，忽视受体因素的影响。利用基因组数据激增所提供的机遇，本项目计划通过比较基因组学分析，发掘细胞核基因组中影响细胞器DNA片段插入的特征，探索核基因组本身变小的进化趋势是否是它们接受细胞器DNA的阻力，探索新转移基因获得剪接体内含子的机制，探讨核基因组中转运肽编码序列丰富度是否影响基因成功转移的频率。综合评估现有理论假说的优缺点，提出新假说、完善细胞器基因组进化的理论。本课题的深入研究，不仅可以揭示真核生物遗传系统多样性的进化基础，而且对跨物种水平基因转移、胞质雄性不育、杂种优势、线粒体缺陷的基因治疗等生物、农业、医学难题的解决具有参考价值。

One of the most prominent features of organelle genome evolution is the massive transfer of their genes to the nucleus. In principle, there are three participants in any gene transfer event: the donor (the organelle genome), the being transferred DNA sequence, and the recipient (the nuclear genome). After extensive survey of the literatures, we found that most of the previous studies were focused on the donors and the being transferred genes but overlooked the effects of the recipients: whether they were liable to accept the foreign DNA sequences and how the organelle genes were adapted to the expression system of the nucleus. Taking the advantage of the explosion of genomic data, we will carry out a series of comparative genomic analyses to explore the characteristics of nuclear genomes that influence the insertion of organelle sequences, and examine whether the nuclear genomes whose own sizes are shrinking in evolution are resistant to the insertion of organelle sequences. In addition, we will study the key steps of the domestication of the organelle genes in the nuclear environment: the gain of spliceosomal introns, the recruitment of transit-peptide coding sequence and their influencing factors. Finally, we will comprehensively evaluate all the current hypotheses of organelle genome evolution and try to construct new hypothesis for next-step studies. The results of this project will contribute to the understanding of the evolutionary basis of eukaryotic genetic diversity and give significant implications to the studies of heterosis, cytoplasmic male sterility, and horizontal gene transfer across species as well as the gene therapy of mitochondrial diseases.