Nonreproductive role of gonadotropin‐releasing hormone in the control of ascidian metamorphosis

• Published in: Developmental dynamics 2014-12, Vol.243 (12), p.1524-1535
• Main Authors: Kamiya, Chisato, Ohta, Naoyuki, Ogura, Yosuke, Yoshida, Keita, Horie, Takeo, Kusakabe, Takehiro G., Satake, Honoo, Sasakura, Yasunori
• Format: Article
• Language: English
• Subjects: Animals; ascidian; Cell Cycle Checkpoints - physiology; Ciona intestinalis - embryology; Cyclic AMP - metabolism; GnRH; Gonadotropin-Releasing Hormone - metabolism; Larva - metabolism; metamorphosis; Metamorphosis, Biological - physiology
• ISSN: 1058-8388; 1097-0177
• DOI: 10.1002/dvdy.24176

Background: Gonadotropin‐releasing hormones (GnRHs) are neuropeptides that play central roles in the reproduction of vertebrates. In the ascidian Ciona intestinalis, GnRHs and their receptors are expressed in the nervous systems at the larval stage, when animals are not yet capable of reproduction, suggesting that the hormones have non‐reproductive roles. Results: We showed that GnRHs in Ciona are involved in the animal′s metamorphosis by regulating tail absorption and adult organ growth. Absorption of the larval tail and growth of the adult organs are two major events in the metamorphosis of ascidians. When larvae were treated with GnRHs, they completed tail absorption more frequently than control larvae. cAMP was suggested to be a second messenger for the induction of tail absorption by GnRHs. tGnRH‐3 and tGnRH‐5 (the “t” indicates “tunicate”) inhibited the growth of adult organs by arresting cell cycle progression in parallel with the promotion of tail absorption. Conclusions: This study provides new insights into the molecular mechanisms of ascidian metamorphosis conducted by non‐reproductive GnRHs. Developmental Dynamics 243:1524–1535, 2014. © 2014 Wiley Periodicals, Inc. Key Findings Ciona GnRHs control the progression of metamorphic events at the larval stage when animals are in a reproductively immature state. GnRHs promote tail absorption. tGnRH‐3 and tGnRH‐5 control cell proliferation during metamorphosis by arresting G1‐S transition.