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虹鳟鱼骨骼肌对拥挤胁迫的分子和表观遗传反应

Molecular and epigenetic responses to crowding stress in rainbow trout () skeletal muscle.

作者信息

Aravena-Canales Daniela, Valenzuela-Muñoz Valentina, Gallardo-Escarate Cristian, Molina Alfredo, Valdés Juan Antonio

机构信息

Laboratorio de Biotecnología Molecular, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile.

Interdisciplinary Center for Aquaculture Research (INCAR), University of Concepción, Concepcion, Chile.

出版信息

Front Endocrinol (Lausanne). 2025 Apr 16;16:1571111. doi: 10.3389/fendo.2025.1571111. eCollection 2025.

DOI:10.3389/fendo.2025.1571111
PMID:40309435
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12040688/
Abstract

BACKGROUND

Chronic stress is a critical challenge in fish aquaculture, adversely affecting growth, health, and overall productivity. Among the most significant chronic stressors in intensive farming is crowding, which triggers the release of cortisol, the primary stress hormone in fish. Cortisol re-allocates energy away from growth-related processes toward stress response mechanisms. Consequently, overcrowded fish often exhibit slower growth rates, and impaired skeletal muscle development. Understanding the mechanisms underlying crowding stress and their long-term effects, including epigenetic changes, is essential for optimizing farming conditions, and enhancing fish welfare.

OBJECTIVE

This study aims to characterize the physiological, transcriptomic, and epigenomic responses in juvenile rainbow trout () exposed for 30 days to high stocking densities.

RESULTS

Crowding stress led to decreased weight in the high-density (HD) group. It also resulted in elevated cortisol levels, oxidative DNA damage, and protein carbonylation in skeletal muscle. Using RNA-seq, we identified 4,050 differentially expressed genes (DEGs), and through whole-genome bisulfite sequencing (WGBS), we detected 11,672 differentially methylated genes (DMGs). Integrative analyses revealed 263 genes with a negative correlation between upregulated expression and downregulated methylation, primarily associated with autophagy, mitophagy, and the insulin signaling pathway. Conversely, 299 genes exhibited the reverse trend, mainly linked to ATP-dependent chromatin remodeling.

CONCLUSION

This study offers the first detailed exploration of the molecular responses in skeletal muscle to crowding stress, integrating RNA-seq and WGBS analysis in rainbow trout, offering valuable information for improving aquaculture practices.

摘要

背景

慢性应激是鱼类养殖中的一项严峻挑战,对生长、健康和整体生产力产生不利影响。集约化养殖中最显著的慢性应激源之一是拥挤,它会引发鱼类主要应激激素皮质醇的释放。皮质醇会将能量从与生长相关的过程重新分配到应激反应机制。因此,过度拥挤的鱼类通常生长速度较慢,骨骼肌发育也会受损。了解拥挤应激的潜在机制及其长期影响,包括表观遗传变化,对于优化养殖条件和提高鱼类福利至关重要。

目的

本研究旨在描述暴露于高放养密度30天的幼年虹鳟鱼的生理、转录组和表观基因组反应。

结果

拥挤应激导致高密度(HD)组体重下降。还导致骨骼肌中皮质醇水平升高、氧化性DNA损伤和蛋白质羰基化。使用RNA测序,我们鉴定出4050个差异表达基因(DEG),并通过全基因组亚硫酸氢盐测序(WGBS),检测到11672个差异甲基化基因(DMG)。综合分析揭示了263个基因,其表达上调与甲基化下调呈负相关,主要与自噬、线粒体自噬和胰岛素信号通路有关。相反,299个基因呈现相反趋势,主要与ATP依赖的染色质重塑有关。

结论

本研究首次详细探讨了骨骼肌对拥挤应激的分子反应,将RNA测序和WGBS分析整合到虹鳟鱼中,为改进水产养殖实践提供了有价值的信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/0f7bf3b7cb16/fendo-16-1571111-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/c8b69f87adcd/fendo-16-1571111-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/4b48bd16ad43/fendo-16-1571111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/836371a948d9/fendo-16-1571111-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/8484e9e9ffe2/fendo-16-1571111-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/82c1c1247fc9/fendo-16-1571111-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/0f7bf3b7cb16/fendo-16-1571111-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/c8b69f87adcd/fendo-16-1571111-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/4b48bd16ad43/fendo-16-1571111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/836371a948d9/fendo-16-1571111-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/8484e9e9ffe2/fendo-16-1571111-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/82c1c1247fc9/fendo-16-1571111-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0759/12040688/0f7bf3b7cb16/fendo-16-1571111-g006.jpg

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