大多數的進化生物學家願意關注物種間同源的基因、結構以及過程是如何出現或者這些性狀如何出現分歧的。但是對於一些形態學特徵以及發育的過程來說，「同源」的定義是有問題的。脊索動物中的變態發育就是一個典型的例子。
最近，一個由來自法國、波蘭、斯洛伐克和美國科學家組成的跨國研究組對文昌魚的變態發育進行了研究。在脊索動物的胚胎後發育過程中，不同的譜系中從幼體到成體存在廣泛的變態發育，這種現象提示我們，這種形態學上的多樣性有可能是通過獨立發生的過程而產生的。在脊椎動物中，變態發育是由甲狀腺激素（THs）和甲狀腺激素受體（TRs）的結合而引發的。科學家通過研究發現，甲狀腺激素的衍生物，一種叫做TRIAC的物質，在頭索動物文昌魚中誘導了變態。文昌魚的甲狀腺素受體由於與TRIAC緊密結合，從而介導了自然發生的和由TRIAC誘導的變態過程。而NH3作為甲狀腺素的拮抗劑，阻止了自然發生的和由TRIAC誘導的變態過程。文昌魚的甲狀腺素受體的表達水平也隨著甲狀腺素的增加而增加。因此，由甲狀腺素誘導的變態過程受到了甲狀腺素受體的調節，這種變態過程是所有脊索動物的祖先特徵，這種調節網絡的保守性也支持變態在脊索動物譜系中是具有同源性的。相關論文發表在《當代生物學》（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, ,
Received 29 October 2007;
revised 17 April 2008;
accepted 25 April 2008.
Published online: May 29, 2008.
Available online 2 June 2008.
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.