研究人員利用斑馬魚找到了一個基因,，正是它使得這條巨大的鏡鯉生有少而大的鱗片,。
長期以來，生物學(xué)研究一直被一個問題所困擾,，那就是進(jìn)化對基因的修修補(bǔ)補(bǔ)為何沒有把生命變得一團(tuán)糟,。一種流行的理論認(rèn)為，基因組拷貝了一些關(guān)鍵的基因,，因此一旦有突變破壞了這些基因,，生物體還留有一個備份。研究人員如今找到了新的證據(jù),，表明進(jìn)化是按照這種方式工作的,。
研究人員追蹤到一種被復(fù)制的基因——在這種基因的作用下能夠繁殖出所謂的鏡子魚,，這些魚擁有巨大且能夠反射光線的鱗片。美國紐約州錫拉丘茲大學(xué)的進(jìn)化生物學(xué)家R. Craig Albertson指出：“這是有關(guān)這種假設(shè)的一個很有價值的證據(jù),，它完美地闡釋了基因和基因組復(fù)制如何推動形態(tài)學(xué)的演化,。”
德國蒂賓根市馬普學(xué)會發(fā)育生物學(xué)研究所的生物學(xué)家Matthew Harris和Nicholas Rohner，通過利用化學(xué)物質(zhì)使斑馬魚的基因產(chǎn)生突變,，進(jìn)而開始了他們的實驗。隨后他們根據(jù)不尋常的特征篩查了發(fā)生突變的斑馬魚,。其中的一個突變便是幾乎全身沒有鱗片,，這不禁使人想起了鏡鯉——為了容易打理而沒有多少鱗片的一種魚——的培育。研究人員最終將這一突變歸結(jié)到一個名為纖維原細(xì)胞生長因子受體1（fgfr1）的基因,。
由于這一基因發(fā)生的突變通常會導(dǎo)致哺乳動物和魚類胚胎的死亡,，因此Harris和Rohner推測，其在斑馬魚基因組中一定也會有一個“孿生兄弟”,。事實果然如此,。除了導(dǎo)致鏡面鱗片的突變版本之外，研究人員還找到了fgfr1的一個無損版本,。
為了研究復(fù)制和突變的過程是否也會發(fā)生在實驗室之外,，Harris和Rohner在鏡鯉體內(nèi)篩查了fgfr1。研究人員最終在兩種鏡鯉中發(fā)現(xiàn)了復(fù)制的fgfr1基因——其中的一個副本丟失了孿生基因所具有的111個堿基,，而另一個副本則有一個堿基與孿生基因不同,。研究人員推測，正是這兩個副本導(dǎo)致了較少的鱗片,。研究小組在9月3日的《當(dāng)代生物學(xué)》（Current Biology）網(wǎng)絡(luò)版上報告了這一研究成果,。
這是Harris和Rohner發(fā)現(xiàn)的第一個經(jīng)過復(fù)制的基因，但是他們希望能夠找到更多這樣的基因,。在斑馬魚的17000多個基因中,，大約有25%的基因都是經(jīng)過復(fù)制的，同時與經(jīng)過馴化的動物一樣,，這些突變也應(yīng)當(dāng)存在于野生動物體內(nèi),。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
