科学家在最新一期的《自然》杂志中报道称，有两个基因在鱼鳍的发育过程中起关键作用，但它们在动物的四肢中却没有出现，失去这两个基因或许是从鱼鳍进化到动物四肢的“关键步骤”。

加拿大渥太华大学玛丽-安德烈-艾金门科领导的团队进行了这项研究。她们从研究斑马鱼胚胎的发育入手，发现了两个关键基因。这两个基因编码的蛋白质对鱼鳍的结构非常重要，它们是角质鳍条的组成部分，角质鳍条在鱼卵中可以看到，随着鱼的不断成熟，它们就发育为多骨的鳍条。

研究人员表示，但在动物的四肢中却没有对应的基因。为了确认这一点，他们在象鼻鲨的基因组中也找到了同样的基因，象鼻鲨是一种非常基础的鱼类，这表明这些古老的基因一直在有骨头的鱼体内存在，这些鱼在进化成四足动物时失去了这些基因。

为了更详细地研究这些变化，科学家控制了斑马鱼的发育过程。他们抑制了一个正在发育的斑马鱼胚胎中的这两个基因的活性，结果发现，该斑马鱼长出了“被截了一段”的较短鱼鳍，而且，鱼鳍上没有多骨的鳍条。

研究人员认为，这表明，失去这些基因是从鱼鳍进化到四肢的一个关键步骤。

该研究团队也将正常的斑马鱼胚胎的发育过程同老鼠胚胎的发育过程相比较。艾金门科表示，鱼鳍的发育同动物四肢的发育最初非常相似，但是，当这两个基因开始表达时，它们的发育开始出现差异。

原文出处：

Nature doi:10.1038/nature09137

Loss of fish actinotrichia proteins and the fin-to-limb transition
Jing Zhang,Purva Wagh,Danielle Guay,Luis Sanchez-Pulido,Bhaja K. Padhi,Vladimir Korzh,Miguel A. Andrade-Navarro& Marie-Andrée Akimenko

The early development of teleost paired fins is strikingly similar to that of tetrapod limb buds and is controlled by similar mechanisms1, 2. One early morphological divergence between pectoral fins and limbs is in the fate of the apical ectodermal ridge (AER), the distal epidermis that rims the bud. Whereas the AER of tetrapods regresses after specification of the skeletal progenitors3, the AER of teleost fishes forms a fold that elongates4, 5. Formation of the fin fold is accompanied by the synthesis of two rows of rigid, unmineralized fibrils called actinotrichia, which keep the fold straight6, 7 and guide the migration of mesenchymal cells within the fold5, 8. The actinotrichia are made of elastoidin, the components of which, apart from collagen, are unknown. Here we show that two zebrafish proteins, which we name actinodin 1 and 2 (And1 and And2), are essential structural components of elastoidin. The presence of actinodin sequences in several teleost fishes and in the elephant shark (Callorhinchus milii, which occupies a basal phylogenetic position), but not in tetrapods, suggests that these genes have been lost during tetrapod species evolution. Double gene knockdown of and1 and and2 in zebrafish embryos results in the absence of actinotrichia and impaired fin folds. Gene expression profiles in embryos lacking and1 and and2 function are consistent with pectoral fin truncation and may offer a potential explanation for the polydactyly observed in early tetrapod fossils. We propose that the loss of both actinodins and actinotrichia during evolution may have led to the loss of lepidotrichia and may have contributed to the fin-to-limb transition.