A young Drosophila duplicate gene plays essential roles in spermatogenesis by regulating several Y-linked male fertility genes.
A young Drosophila duplicate gene plays essential roles in spermatogenesis by regulating several Y-linked male fertility genes.
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DOI：
10.1371/journal.pgen.1001255
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发表时间：
2010-12-23
期刊：
影响因子：
4.5
通讯作者：
Wang W
中科院分区：
文献类型：
--
作者：
Ding Y;Zhao L;Yang S;Jiang Y;Chen Y;Zhao R;Zhang Y;Zhang G;Dong Y;Yu H;Zhou Q;Wang W
基因复制被认为是基因创新的主要来源。然而，一个新的重复基因如何通过整合到一个途径中获得功能，并导致适应性重要的表型仍然是未知的。本文通过对果蝇（Drosophila melanogaster）种亚群中年轻kep1基因家族的生物学作用及其分子机制的研究，旨在了解具有新功能的新基因的起源和进化。序列和表达分析表明，其中一个新的重复基因nsr（novel spermatogenesis regulator）具有正选择信号和新的亚细胞定位模式。靶向诱变和全转录组测序分析提供的证据表明，NSR是男性生殖所必需的，与精子个体化，卷曲和精子轴丝的结构完整性通过转录后调节几个Y染色体育性基因。在复制前的果蝇种yakuba中，没有类似于NSR的表达模式，并且存在亲本基因kep1的相应顺式调控元件，这表明kep1可能不是祖先所需的雄性功能，并且NSR可能经历了新功能化过程，这是由反式调控库的变化促成的。这些发现不仅全面地展示了一个新的重复基因的进化过程，而且表明最近起源的重复基因可以通过调节必需基因来获得多种生物学功能并建立新的功能途径。基因复制长期以来一直被认为是新基因和新功能的主要来源。然而，新的重复基因如何在功能上整合到现有的基因网络中，以及它们如何在途径水平上对生物体的新功能做出贡献，仍然是一个迷人的谜。通过对果蝇（Drosophilamelanogaster）中最近发现的kep1基因家族的研究，我们发现，其中一个年轻的重复基因NSR在其诞生后的短暂进化期内，通过调控几个必需的育性基因，进化出了与雄性生殖相关的重要生物学功能。本研究揭示了nsr的进化动力学、生物学作用和潜在的分子机制，为新基因如何获得重要的生物学功能提供了一个生动而全面的例子，并证明了新近产生的新基因可以调控先前存在的必需基因，创造新的遗传途径结构。
Gene duplication is supposed to be the major source for genetic innovations. However, how a new duplicate gene acquires functions by integrating into a pathway and results in adaptively important phenotypes has remained largely unknown. Here, we investigated the biological roles and the underlying molecular mechanism of the young kep1 gene family in the Drosophila melanogaster species subgroup to understand the origin and evolution of new genes with new functions. Sequence and expression analysis demonstrates that one of the new duplicates, nsr (novel spermatogenesis regulator), exhibits positive selection signals and novel subcellular localization pattern. Targeted mutagenesis and whole-transcriptome sequencing analysis provide evidence that nsr is required for male reproduction associated with sperm individualization, coiling, and structural integrity of the sperm axoneme via regulation of several Y chromosome fertility genes post-transcriptionally. The absence of nsr-like expression pattern and the presence of the corresponding cis-regulatory elements of the parental gene kep1 in the pre-duplication species Drosophila yakuba indicate that kep1 might not be ancestrally required for male functions and that nsr possibly has experienced the neofunctionalization process, facilitated by changes of trans-regulatory repertories. These findings not only present a comprehensive picture about the evolution of a new duplicate gene but also show that recently originated duplicate genes can acquire multiple biological roles and establish novel functional pathways by regulating essential genes. Gene duplication has long been appreciated as a major source for new genes and new functions. Nevertheless, it is still a fascinating mystery how new duplicate genes are functionally integrated into the existing gene network and how they contribute to the novel functions of organisms at the pathway level. By studying the recently originated kep1 gene family in Drosophila melanogaster, we show that one of the young duplicate genes, nsr, has evolved important biological functions associated with male reproduction by regulating several essential fertility genes in the short evolutionary period after its birth. The evolutionary dynamics, biological roles, and the underlying molecular mechanism of nsr revealed in this study present a vivid and comprehensive example of how new genes acquire important biological functions and demonstrate that recently originated new genes can regulate pre-existing essential genes and create novel architectures of genetic pathways.
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影响因子：
1.6
作者：
HARDY, RW;TOKUYASU, KT;LINDSLEY, DL
通讯作者：
LINDSLEY, DL
DOI：
10.1038/nrg2487
发表时间：
2009-01
期刊：
Nature reviews. Genetics
影响因子：
--
作者：
通讯作者：
--
影响因子：
44.1
作者：
Li, Dan;Dong, Yang;Wang, Wen
通讯作者：
Wang, Wen
影响因子：
7
作者：
Heger, Andreas;Ponting, Chris P.
通讯作者：
Ponting, Chris P.
影响因子：
9.2
作者：
Loppin, B;Lepetit, D;Karr, TL
通讯作者：
Karr, TL