大多數(shù)的進(jìn)化生物學(xué)家愿意關(guān)注物種間同源的基因、結(jié)構(gòu)以及過(guò)程是如何出現(xiàn)或者這些性狀如何出現(xiàn)分歧的,。但是對(duì)于一些形態(tài)學(xué)特征以及發(fā)育的過(guò)程來(lái)說(shuō)，“同源”的定義是有問(wèn)題的,。脊索動(dòng)物中的變態(tài)發(fā)育就是一個(gè)典型的例子。
最近,，一個(gè)由來(lái)自法國(guó),、波蘭、斯洛伐克和美國(guó)科學(xué)家組成的跨國(guó)研究組對(duì)文昌魚(yú)的變態(tài)發(fā)育進(jìn)行了研究,。在脊索動(dòng)物的胚胎后發(fā)育過(guò)程中,，不同的譜系中從幼體到成體存在廣泛的變態(tài)發(fā)育，這種現(xiàn)象提示我們,，這種形態(tài)學(xué)上的多樣性有可能是通過(guò)獨(dú)立發(fā)生的過(guò)程而產(chǎn)生的,。在脊椎動(dòng)物中，變態(tài)發(fā)育是由甲狀腺激素（THs）和甲狀腺激素受體（TRs）的結(jié)合而引發(fā)的,?？茖W(xué)家通過(guò)研究發(fā)現(xiàn)，甲狀腺激素的衍生物，一種叫做TRIAC的物質(zhì),，在頭索動(dòng)物文昌魚(yú)中誘導(dǎo)了變態(tài),。文昌魚(yú)的甲狀腺素受體由于與TRIAC緊密結(jié)合，從而介導(dǎo)了自然發(fā)生的和由TRIAC誘導(dǎo)的變態(tài)過(guò)程,。而NH3作為甲狀腺素的拮抗劑,，阻止了自然發(fā)生的和由TRIAC誘導(dǎo)的變態(tài)過(guò)程。文昌魚(yú)的甲狀腺素受體的表達(dá)水平也隨著甲狀腺素的增加而增加,。因此,，由甲狀腺素誘導(dǎo)的變態(tài)過(guò)程受到了甲狀腺素受體的調(diào)節(jié)，這種變態(tài)過(guò)程是所有脊索動(dòng)物的祖先特征,，這種調(diào)節(jié)網(wǎng)絡(luò)的保守性也支持變態(tài)在脊索動(dòng)物譜系中是具有同源性的,。相關(guān)論文發(fā)表在《當(dāng)代生物學(xué)》（Current Biology）上。（生物谷Bioon.com）
生物谷推薦原始出處：
Current Biology,，Volume 18, Issue 11, 3 June 2008, Pages 825-830,，Mathilde Paris，Vincent Laudet
Amphioxus Postembryonic Development Reveals the Homology of Chordate Metamorphosis
Mathilde Paris1, Hector Escriva2, Michael Schubert1, Frédéric Brunet1, Julius Brtko3, Fabrice Ciesielski4, Dominique Roecklin4, Valérie Vivat-Hannah4, Emilien L. Jamin5, Jean-Pierre Cravedi5, Thomas S. Scanlan6, Jean-Paul Renaud4, Nicholas D. Holland7 and Vincent Laudet1, ,
1Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, CNRS, INRA, UCB Lyon 1, IFR128 Lyon Biosciences, Ecole Normale Supérieure de Lyon, 69364 Lyon Cedex 07, France
2Laboratoire Arago, UMR-7628, CNRS, University Pierre and Marie Curie, 66651 Banyuls sur Mer, France
3Institute of Experimental Endocrinology, Slovak Academy of Sciences, 833 06 Bratislava, Slovak Republic
4AliX, Boulevard Sébastien Brant, Parc d'Innovation, 67400 Illkirch, France
5INRA, UMR-1089 Xenobiotiques, 31931 Toulouse Cedex 9, France
6Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239
7Marine Biology Research Division, Scripps Institution of Oceanography, University of California, San Diego, La Jolla, California 92093-0202
Received 29 October 2007; revised 17 April 2008; accepted 25 April 2008. Published online: May 29, 2008. Available online 2 June 2008.
Summary
Most studies in evolution are centered on how homologous genes, structures, and/or processes appeared and diverged. Although historical homology is well defined as a concept, in practice its establishment can be problematic, especially for some morphological traits or developmental processes. Metamorphosis in chordates is such an enigmatic character. Defined as a spectacular postembryonic larva-to-adult transition, it shows a wide morphological diversity between the different chordate lineages, suggesting that it might have appeared several times independently. In vertebrates, metamorphosis is triggered by binding of the thyroid hormones (THs) T4 and T3 to thyroid-hormone receptors (TRs). Here we show that a TH derivative, triiodothyroacetic acid (TRIAC), induces metamorphosis in the cephalochordate amphioxus. The amphioxus TR (amphiTR) mediates spontaneous and TRIAC-induced metamorphosis because it strongly binds to TRIAC, and a specific TR antagonist, NH3, inhibits both spontaneous and TRIAC-induced metamorphosis. Moreover, as in amphibians, amphiTR expression levels increase around metamorphosis and are enhanced by THs. Therefore, TH-regulated metamorphosis, mediated by TR, is an ancestral feature of all chordates. This conservation of a regulatory network supports the homology of metamorphosis in the chordate lineage.
