科學(xué)家在最新一期的《自然》雜志中報(bào)道稱，有兩個(gè)基因在魚鰭的發(fā)育過程中起關(guān)鍵作用,，但它們?cè)趧?dòng)物的四肢中卻沒有出現(xiàn),，失去這兩個(gè)基因或許是從魚鰭進(jìn)化到動(dòng)物四肢的“關(guān)鍵步驟”。
加拿大渥太華大學(xué)瑪麗-安德烈-艾金門科領(lǐng)導(dǎo)的團(tuán)隊(duì)進(jìn)行了這項(xiàng)研究,。她們從研究斑馬魚胚胎的發(fā)育入手,，發(fā)現(xiàn)了兩個(gè)關(guān)鍵基因。這兩個(gè)基因編碼的蛋白質(zhì)對(duì)魚鰭的結(jié)構(gòu)非常重要,，它們是角質(zhì)鰭條的組成部分,，角質(zhì)鰭條在魚卵中可以看到,，隨著魚的不斷成熟，它們就發(fā)育為多骨的鰭條,。
研究人員表示,，但在動(dòng)物的四肢中卻沒有對(duì)應(yīng)的基因。為了確認(rèn)這一點(diǎn),，他們?cè)谙蟊酋彽幕蚪M中也找到了同樣的基因,，象鼻鯊是一種非常基礎(chǔ)的魚類,，這表明這些古老的基因一直在有骨頭的魚體內(nèi)存在,，這些魚在進(jìn)化成四足動(dòng)物時(shí)失去了這些基因。
為了更詳細(xì)地研究這些變化,，科學(xué)家控制了斑馬魚的發(fā)育過程,。他們抑制了一個(gè)正在發(fā)育的斑馬魚胚胎中的這兩個(gè)基因的活性,，結(jié)果發(fā)現(xiàn),，該斑馬魚長出了“被截了一段”的較短魚鰭,，而且，魚鰭上沒有多骨的鰭條,。
研究人員認(rèn)為，這表明,，失去這些基因是從魚鰭進(jìn)化到四肢的一個(gè)關(guān)鍵步驟,。
該研究團(tuán)隊(duì)也將正常的斑馬魚胚胎的發(fā)育過程同老鼠胚胎的發(fā)育過程相比較。艾金門科表示,，魚鰭的發(fā)育同動(dòng)物四肢的發(fā)育最初非常相似,，但是，當(dāng)這兩個(gè)基因開始表達(dá)時(shí),，它們的發(fā)育開始出現(xiàn)差異,。(生物谷www.Bioon.net)
生物谷推薦原文出處：
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.
