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视黄酸依赖性海星变态的作用机制。

Mechanism underlying retinoic acid-dependent metamorphosis in the starfish.

机构信息

Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8572, Japan.

Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Ibaraki, 305-8577, Japan.

出版信息

Dev Biol. 2022 Dec;492:119-125. doi: 10.1016/j.ydbio.2022.10.002. Epub 2022 Oct 12.

DOI:10.1016/j.ydbio.2022.10.002
PMID:36240875
Abstract

The evolution of the biphasic life cycle in marine invertebrates has attracted considerable interest in zoology. We recently provided evidence that retinoic acid (RA) is involved in the regulation of metamorphosis in starfish. It also functions in life cycle transitions of jellyfish (cnidaria). Thus, documenting the evolutionarily conserved role of RA in such transitions will help to trace the life cycle evolution of bilaterians and cnidarians. In this study, we examined the molecular mechanisms by which RA signaling is involved in the commencement of metamorphosis in starfish. First, we measured RA levels during the larval and metamorphosis stages by liquid chromatography-tandem mass spectrometry. We found that all-trans RA levels in the larval body are high before larvae acquire competence for metamorphosis, suggesting that the commencement of metamorphosis is not controlled by increased RA synthesis. Furthermore, the suppression of rar gene expression by TALEN-mediated gene knockout revealed that RA receptor (RAR) is essential for metamorphosis. These observations suggest that the initiation of metamorphosis is regulated at the level of synthesized RA to activate RAR. We discuss the divergence of ligand molecules and receptors during the evolution of life cycle regulation.

摘要

海洋无脊椎动物双相生活史的进化在动物学中引起了相当大的兴趣。我们最近提供的证据表明,视黄酸(RA)参与了海星变态的调节。它也在水母(刺胞动物)的生活史转变中起作用。因此,记录 RA 在这些转变中的进化保守作用将有助于追踪两侧对称动物和刺胞动物的生活史进化。在这项研究中,我们研究了 RA 信号参与海星变态开始的分子机制。首先,我们通过液相色谱-串联质谱法测量了幼虫和变态阶段的 RA 水平。我们发现,在幼虫获得变态能力之前,幼虫体内的全反式 RA 水平很高,这表明变态的开始不受 RA 合成增加的控制。此外,TALEN 介导的基因敲除抑制 rar 基因表达表明 RA 受体(RAR)对变态是必需的。这些观察结果表明,变态的启动受合成 RA 水平的调节以激活 RAR。我们讨论了在生活史调控进化过程中配体分子和受体的分歧。

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Activation of retinoic acid receptor-dependent transcription by all-trans-retinoic acid metabolites and isomers.全反式维甲酸代谢物和异构体对维甲酸受体依赖性转录的激活作用。
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The endogenous retinoid metabolite S-4-oxo-9-cis-13,14-dihydro-retinoic acid activates retinoic acid receptor signalling both in vitro and in vivo.内源性类视黄醇代谢物S-4-氧代-9-顺式-13,14-二氢视黄酸在体外和体内均可激活视黄酸受体信号通路。
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