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NMDAR-CaMKII通路作为攻击行为的核心调节因子:来自梭子蟹转录组学和代谢组学分析的证据

NMDAR-CaMKII Pathway as a Central Regulator of Aggressiveness: Evidence from Transcriptomic and Metabolomic Analysis in Swimming Crabs .

作者信息

Liang Qihang, Liu Dapeng, Zhu Boshan, Wang Fang

机构信息

Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266003, China.

Function Laboratory for Marine Fisheries Science and Food Production Processes, Laoshan Laboratory, Qingdao 266237, China.

出版信息

Int J Mol Sci. 2024 Nov 22;25(23):12560. doi: 10.3390/ijms252312560.

Abstract

Aggressiveness is one of the personality traits of crustaceans, playing a crucial role in their growth, life history, and adaptability by influencing resource acquisition. However, the neuroregulatory mechanisms of aggressiveness in crustaceans remain poorly understood. The thoracic ganglion offers valuable insights into complementary aspects of aggression control. This study identified the aggressiveness of swimming crabs , conducted transcriptomic and metabolomic analyses of the thoracic ganglia, and confirmed the neural regulatory effects on aggressiveness. Behavioral analyses showed that highly aggressive individuals exhibited increased frequency and duration of chela extension, more frequent attacks, approaches and retreats, as well as extended movement distances. Omics analysis revealed 11 key candidate genes and three metabolites associated with aggressiveness, which were primarily enriched in pathways related to energy metabolism and neurodegeneration. Injection of an NMDAR activator significantly decreased aggressiveness in highly aggressive crabs, accompanied by a significant increase in NMDAR protein fluorescence intensity and downregulation of , , and genes. Conversely, when lowly aggressive crabs were injected with an NMDAR inhibitor, they showed increased aggressiveness alongside significantly decreased NMDAR protein fluorescence intensity, upregulated expression, and downregulated and genes. These results suggest that NMDAR within the thoracic ganglia serves as a key receptor in modulating aggressiveness in , potentially by influencing neural energy state via the NMDAR-CaMKII pathway, which in turn affects oxidative phosphorylation, cAMP, and FoxO pathways.

摘要

攻击性是甲壳类动物的个性特征之一,通过影响资源获取在其生长、生活史和适应性方面发挥着关键作用。然而,甲壳类动物攻击性的神经调节机制仍知之甚少。胸神经节为攻击控制的补充方面提供了有价值的见解。本研究确定了梭子蟹的攻击性,对胸神经节进行了转录组学和代谢组学分析,并证实了对攻击性的神经调节作用。行为分析表明,高攻击性个体的螯伸展频率和持续时间增加,攻击、接近和撤退更频繁,移动距离也更长。组学分析揭示了11个与攻击性相关的关键候选基因和三种代谢物,它们主要富集在与能量代谢和神经退行性变相关的途径中。注射NMDAR激活剂显著降低了高攻击性螃蟹的攻击性,同时NMDAR蛋白荧光强度显著增加,以及 、 和 基因的下调。相反,当向低攻击性螃蟹注射NMDAR抑制剂时,它们的攻击性增加,同时NMDAR蛋白荧光强度显著降低, 表达上调, 和 基因下调。这些结果表明,胸神经节内的NMDAR可能通过NMDAR-CaMKII途径影响神经能量状态,进而影响氧化磷酸化、cAMP和FoxO途径,从而成为调节梭子蟹攻击性的关键受体。

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