Investigating the role of myoinhibitory peptide (MIP) signalling in marine larval settlement and metamorphosis. (ref: 4281)
研究肌抑制肽 (MIP) 信号在海洋幼虫定居和变态中的作用。
基本信息
- 批准号:2706100
- 负责人:
- 金额:--
- 依托单位:
- 依托单位国家:英国
- 项目类别:Studentship
- 财政年份:2022
- 资助国家:英国
- 起止时间:2022 至 无数据
- 项目状态:未结题
- 来源:
- 关键词:
项目摘要
In animal nervous systems, neuropeptides are key agents of change. These peptidergic signalling molecules are used to regulate a plethora of biological processes, including reproduction, circadian cycles, behaviour, digestion and excretion.The process of metamorphosis, where dramatic changes in behaviour, physiology and morphology occur within a relatively short time period, is an excellent system with which to study how neuropeptide signalling systems activate or inhibit change in a biological system. In this project, we aim to explore the neuropeptidergic regulation of larval settlement and metamorphosis in the larvae of two different marine invertebrates, the nereid polychaete Platynereis dumerilii, and the Pacific Oyster Crassostrea gigas. We will focus on a neuropeptide known to induce settlement in Platynereis, myoinhibitory peptide (MIP), which was recently found to signal through two different types of receptor, the MIP-gated ion channel (MGIC) and the MIP-activated G protein-coupled receptor (MAG).Through the establishment of MIP receptor mutant lines in Platynereis, we will investigate the contributions of each receptor type to the larval settlement process. To establish whether the function of MIP in larval settlement and metamorphosis is conserved among other marine invertebrates, we will investigate the expression dynamics of MIP and its receptors during larval development in the Pacific Oyster and test the effect of synthetic MIP peptide on oyster larval development, behaviour and metamorphosis. Results from this project will help to explain how and why neuropeptides signal through multiple receptor types and will increase our understanding of the evolution of neuropeptide signalling. We will also assess whether MIP signalling can be exploited in the context of sustainable aquaculture to enhance and synchronize levels of larval recruitment and growth. Through this PhD project, the student will gain experience in (1) marine invertebrate culture, reproduction and development, (2) genome editing using the CRISPR/Cas9 system, (3) molecular biology techniques including in situ hybridization and immunohistochemistry, (4) neuroethology and physiology (calcium imaging), and (5) fluorescent confocal microscopy.The student will also benefit from training in experimental design, data analysis, critical thinking, scientific writing and communication.
在动物神经系统中,神经肽是变化的关键因素。这些肽能信号分子被用于调节多种生物过程,包括生殖、昼夜节律周期、行为、消化和排泄。变态过程在相对较短的时间内发生行为、生理和形态的巨大变化,是研究神经肽信号系统如何激活或抑制生物系统变化的绝佳系统。在这个项目中,我们的目标是探索两种不同的海洋无脊椎动物,沙蚕多毛类Platynereis dumerilii和太平洋牡蛎的幼虫的定居和变态的神经肽调节。本研究将重点研究一种能够诱导扁水母类幼虫附着的神经肽--肌抑制肽(myoinhibitory peptide,MIP),该肽通过MIP门控离子通道(MGIC)和MIP激活的G蛋白偶联受体(MAG)两种不同类型的受体传递信号,并通过建立扁水母类MIP受体突变体系,研究每种受体类型在幼虫附着过程中的作用。为了确定MIP在幼虫定居和变态中的功能是否在其他海洋无脊椎动物中是保守的,我们将研究MIP及其受体在太平洋牡蛎幼虫发育过程中的表达动态,并测试合成的MIP肽对牡蛎幼虫发育、行为和变态的影响。该项目的结果将有助于解释神经肽如何以及为什么通过多种受体类型发出信号,并将增加我们对神经肽信号进化的理解。我们还将评估MIP信号是否可以在可持续水产养殖的背景下利用,以提高和同步幼虫招募和生长的水平。通过这个博士项目,学生将获得(1)海洋无脊椎动物的培养,繁殖和发育,(2)使用CRISPR/Cas9系统进行基因组编辑,(3)分子生物学技术,包括原位杂交和免疫组织化学,(4)神经行为学和生理学(钙成像),和(5)荧光共聚焦显微镜。学生还将受益于实验设计,数据分析,批判性思维,科学写作和沟通的培训。
项目成果
期刊论文数量(0)
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其他文献
吉治仁志 他: "トランスジェニックマウスによるTIMP-1の線維化促進機序"最新医学. 55. 1781-1787 (2000)
Hitoshi Yoshiji 等:“转基因小鼠中 TIMP-1 的促纤维化机制”现代医学 55. 1781-1787 (2000)。
- DOI:
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LiDAR Implementations for Autonomous Vehicle Applications
- DOI:
- 发表时间:
2021 - 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
吉治仁志 他: "イラスト医学&サイエンスシリーズ血管の分子医学"羊土社(渋谷正史編). 125 (2000)
Hitoshi Yoshiji 等人:“血管医学与科学系列分子医学图解”Yodosha(涉谷正志编辑)125(2000)。
- DOI:
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Effect of manidipine hydrochloride,a calcium antagonist,on isoproterenol-induced left ventricular hypertrophy: "Yoshiyama,M.,Takeuchi,K.,Kim,S.,Hanatani,A.,Omura,T.,Toda,I.,Akioka,K.,Teragaki,M.,Iwao,H.and Yoshikawa,J." Jpn Circ J. 62(1). 47-52 (1998)
钙拮抗剂盐酸马尼地平对异丙肾上腺素引起的左心室肥厚的影响:“Yoshiyama,M.,Takeuchi,K.,Kim,S.,Hanatani,A.,Omura,T.,Toda,I.,Akioka,
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- 影响因子:0
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