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比较转录组、超微结构和组织学分析为华南鲤(Cyprinus carpio rubrofuscus)生长停滞的潜在机制提供了见解。

Comparative transcriptome, ultrastructure and histology analyses provide insights into the potential mechanism of growth arrest in south China carp (Cyprinus carpio rubrofuscus).

作者信息

Zhong Zaixuan, Fan Jiajia, Tian Yuanyuan, Zhu Huaping, Ma Dongmei

机构信息

Pearl River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, Guangdong, China.

Key Laboratory of Tropical and Subtropical Fishery Resources Application and Cultivation, Ministry of Agriculture and Rural Affairs, Guangzhou, Guangdong, China.

出版信息

BMC Genomics. 2024 Dec 2;25(1):1164. doi: 10.1186/s12864-024-11081-9.

DOI:10.1186/s12864-024-11081-9
PMID:39623342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11610312/
Abstract

BACKGROUND

South China carp (Cyprinus carpio rubrofuscus), which is an economically important species, is traditionally cocultured with rice. Our previous study indicated that approximately 10-30% of these fish experienced growth arrest, severely impacting production. However, the molecular mechanism underlying growth inhibition in south China carp is currently unknown.

RESULTS

In this study, we compared the transcriptomes of the livers, muscles and intestines of carp in the fast-growing and slow-growing groups. We identified 2182, 2355 and 916 differentially expressed genes (DEGs), respectively. In the slow-growing group, the oxidative phosphorylation pathway was significantly upregulated in the liver. Transmission electron microscopy (TEM) confirmed mitochondrial damage in the liver, which was characterized by broken cristae and heterogeneous matrix. Additionally, analysis of antioxidant enzyme and transaminase activity also revealed that the livers in slow-growing individuals were unhealthy. In muscle tissue, the mitophagy and autophagy pathways were significantly dysregulated. Consequently, manifestations of mitochondrial damage and sparse myofilaments were clearly observed in slow-growing south China carp via TEM. Furthermore, pathways that regulate cell proliferation and migration, including the ECM receptor and focal adhesion, were significantly enriched in the intestine. Morphological examination revealed that the villus height and muscular layer height in the slow-growing group were significantly shorter than those in the fast-growing group, suggesting decreased intestinal cell motility. Overall, our study elucidated mitochondrial damage in the liver and muscle and detected morphological changes in intestinal villi.

CONCLUSIONS

In summary, our results help elucidate the genetic architecture related to growth arrest in south China carp and provide a basis for further research on the growth of teleosts.

摘要

背景

华南鲤(Cyprinus carpio rubrofuscus)是一种具有重要经济价值的鱼类,传统上与水稻混养。我们之前的研究表明,约10%-30%的这种鱼生长停滞,严重影响产量。然而,华南鲤生长抑制的分子机制目前尚不清楚。

结果

在本研究中,我们比较了快速生长组和缓慢生长组鲤鱼肝脏、肌肉和肠道的转录组。我们分别鉴定出2182、2355和916个差异表达基因(DEG)。在缓慢生长组中,肝脏中的氧化磷酸化途径显著上调。透射电子显微镜(TEM)证实肝脏中的线粒体受损,其特征为嵴断裂和基质不均一。此外,对抗氧化酶和转氨酶活性的分析还表明,缓慢生长个体的肝脏不健康。在肌肉组织中,线粒体自噬和自噬途径显著失调。因此,通过TEM在缓慢生长的华南鲤中清楚地观察到线粒体损伤和肌丝稀疏的表现。此外,包括细胞外基质(ECM)受体和粘着斑在内的调节细胞增殖和迁移的途径在肠道中显著富集。形态学检查显示,缓慢生长组的绒毛高度和肌层高度明显短于快速生长组,表明肠道细胞运动性降低。总体而言,我们的研究阐明了肝脏和肌肉中的线粒体损伤,并检测到肠绒毛的形态变化。

结论

总之,我们的结果有助于阐明与华南鲤生长停滞相关的遗传结构,并为硬骨鱼生长的进一步研究提供基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/e04caea1a0bd/12864_2024_11081_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/42e6087bd977/12864_2024_11081_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/3bf5d8e0036d/12864_2024_11081_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/6f6b402688ca/12864_2024_11081_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/58ed6c347c87/12864_2024_11081_Fig5_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/83900cbee067/12864_2024_11081_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/e04caea1a0bd/12864_2024_11081_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/42e6087bd977/12864_2024_11081_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/3bf5d8e0036d/12864_2024_11081_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/81d62f0e9e83/12864_2024_11081_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/6f6b402688ca/12864_2024_11081_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/58ed6c347c87/12864_2024_11081_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/2e0b927d2650/12864_2024_11081_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/83900cbee067/12864_2024_11081_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bb5/11610312/e04caea1a0bd/12864_2024_11081_Fig8_HTML.jpg

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