研究人员利用斑马鱼找到了一个基因,正是它使得这条巨大的镜鲤生有少而大的鳞片。
长期以来,生物学研究一直被一个问题所困扰,那就是进化对基因的修修补补为何没有把生命变得一团糟。一种流行的理论认为,基因组拷贝了一些关键的基因,因此一旦有突变破坏了这些基因,生物体还留有一个备份。研究人员如今找到了新的证据,表明进化是按照这种方式工作的。
研究人员追踪到一种被复制的基因——在这种基因的作用下能够繁殖出所谓的镜子鱼,这些鱼拥有巨大且能够反射光线的鳞片。美国纽约州锡拉丘兹大学的进化生物学家R. Craig Albertson指出:“这是有关这种假设的一个很有价值的证据,它完美地阐释了基因和基因组复制如何推动形态学的演化。”
德国蒂宾根市马普学会发育生物学研究所的生物学家Matthew Harris和Nicholas Rohner,通过利用化学物质使斑马鱼的基因产生突变,进而开始了他们的实验。随后他们根据不寻常的特征筛查了发生突变的斑马鱼。其中的一个突变便是几乎全身没有鳞片,这不禁使人想起了镜鲤——为了容易打理而没有多少鳞片的一种鱼——的培育。研究人员最终将这一突变归结到一个名为纤维原细胞生长因子受体1(fgfr1)的基因。
由于这一基因发生的突变通常会导致哺乳动物和鱼类胚胎的死亡,因此Harris和Rohner推测,其在斑马鱼基因组中一定也会有一个“孪生兄弟”。事实果然如此。除了导致镜面鳞片的突变版本之外,研究人员还找到了fgfr1的一个无损版本。
为了研究复制和突变的过程是否也会发生在实验室之外,Harris和Rohner在镜鲤体内筛查了fgfr1。研究人员最终在两种镜鲤中发现了复制的fgfr1基因——其中的一个副本丢失了孪生基因所具有的111个碱基,而另一个副本则有一个碱基与孪生基因不同。研究人员推测,正是这两个副本导致了较少的鳞片。研究小组在9月3日的《当代生物学》(Current Biology)网络版上报告了这一研究成果。
这是Harris和Rohner发现的第一个经过复制的基因,但是他们希望能够找到更多这样的基因。在斑马鱼的17000多个基因中,大约有25%的基因都是经过复制的,同时与经过驯化的动物一样,这些突变也应当存在于野生动物体内。(生物谷Bioon.com)
生物谷推荐原始出处:
Current Biology, 03 September 2009 doi:10.1016/j.cub.2009.07.065
Duplication of fgfr1 Permits Fgf Signaling to Serve as a Target for Selection during Domestication
Nicolas Rohner1,,,Miklós Bercsényi2,László Orbán3,4,Maria E. Kolanczyk5,Dirk Linke1,Michael Brand5,Christiane Nüsslein-Volhard1andMatthew P. Harris1,,
1 Max Planck Institute for Developmental Biology, Spemannstrasse 35, 72076 Tübingen, Germany
2 Georgikon Faculty of Agriculture, University of Pannonia, 16 Deák F. Street, H-8361 Keszthely, Hungary
3 Reproductive Genomics Group, Strategic Research Program, Temasek Life Sciences Laboratory, 1 Research Link, National University of Singapore, Singapore 117604
4 Department of Biological Sciences, National University of Singapore, 14 Science Drive 4, Singapore 117543
5 Biotechnologisches Zentrum, Center for Regenerative Therapies Dresden, Technische Universit?t Dresden, Tatzberg 47/49, 01307 Dresden, Germany
The genetic basis of morphological variation both within and between species has been a lasting question in evolutionary biology and one of considerable recent debate [1,2,3]. It is thought that changes in postembryonic development leading to variations in adult form often serve as a basis for selection [4,5,6]. Thus, we investigated the genetic basis of the development of adult structures in the zebrafish via a forward genetic approach and asked whether the genes and mechanisms found could be predictive of changes in other species [7,8]. Here we describe the spiegeldanio (spd) zebrafish mutation, which leads to reduced scale formation in the adult. The affected gene is fibroblast growth factor receptor 1 (fgfr1), which is known to have an essential embryonic function in vertebrate development [9,10]. We find that the zebrafish has two paralogs encoding Fgfr1 and show that they function redundantly during embryogenesis. However, only one paralog is required for formation of scales during juvenile development. Furthermore, we identify loss-of-function alleles changing the coding sequence of Fgfr1a1 that have been independently selected twice during the domestication of the carp (Cyprinus carpio) [11]. These findings provide evidence for the role for gene duplication in providing the raw material for generation of morphological diversity.