Suppr超能文献

转录组学和代谢组学的综合应用为研究凡纳滨对虾抗急性肝胰腺坏死病提供了新视角。

Integrated application of transcriptomics and metabolomics provides insights into acute hepatopancreatic necrosis disease resistance of Pacific white shrimp .

机构信息

Chinese Academy of Sciences (CAS) and Shandong Province Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences , Qingdao, China.

Center for Ocean Mega-Science, Chinese Academy of Sciences , Qingdao, China.

出版信息

mSystems. 2023 Aug 31;8(4):e0006723. doi: 10.1128/msystems.00067-23. Epub 2023 Jun 26.

Abstract

Acute hepatopancreatic necrosis disease (AHPND) has caused a huge economic loss to shrimp aquaculture. (Vp) is regarded as a major causative agent of AHPND in the Pacific white shrimp . However, knowledge about how shrimp resist to AHPND is very limited. In order to learn the molecular mechanisms underlying AHPND resistance of shrimp, comparison between disease-resistant family and susceptible family of were performed at transcriptional and metabolic levels. Integrated analysis of transcriptomics and metabolomics on hepatopancreas of shrimp, the target tissue of Vp, showed that significant differences existed between resistant family and susceptible family of shrimp. The susceptible family showed higher level of glycolysis, serine-glycine metabolism, purine and pyrimidine metabolism, but lower level of betaine-homocysteine metabolism in the hepatopancreas in comparison with the resistant family without Vp infection. Curiously, Vp infection induced up-regulation of glycolysis, serine-glycine metabolism, purine metabolism, pyrimidine metabolism, and pentose phosphate pathway, and down-regulation of betaine-homocysteine metabolism in resistant family. In addition, arachidonic acid metabolism and some immune pathways, like NF-κB and cAMP pathways, were up-regulated in the resistant family after Vp infection. In contrast, amino acid catabolism boosted via PEPCK-mediated TCA cycle flux was activated in the susceptible family after Vp infection. These differences in transcriptome and metabolome between resistant family and susceptible family might contribute to the resistance of shrimp to bacteria. IMPORTANCE (Vp) is a major aquatic pathogen causing acute hepatopancreatic necrosis disease (AHPND) and leads to a huge economic loss to shrimp aquaculture. Despite the recent development of controlling culture environment, disease resistant broodstock breeding is still a sustainable approach for aquatic disease control. Metabolic changes occurred during Vp infection, but knowledge about the metabolism in resistance to AHPND is very limited. Integrated analysis of transcriptome and metabolome revealed the basal metabolic differences exhibited between disease-resistant and susceptible shrimp. Amino acid catabolism might contribute to the pathogenesis of Vp and arachidonic acid metabolism might be responsible for the resistance phenotype. This study will help to enlighten the metabolic and molecular mechanisms underlying shrimp resistance to AHPND. Also, the key genes and metabolites of amino acid and arachidonic acid pathway identified in this study will be applied for disease resistance improvement in the shrimp culture industry.

摘要

急性肝胰腺坏死病(AHPND)给对虾养殖业造成了巨大的经济损失。(Vp)被认为是对虾太平洋白虾 AHPND 的主要病原体。然而,对虾对 AHPND 的抗性的了解非常有限。为了了解对虾对 AHPND 抗性的分子机制,在转录和代谢水平上对抗性家系和易感家系进行了比较。对虾肝胰腺的转录组学和代谢组学的综合分析表明,抗性家系和易感家系之间存在显著差异。与未感染 Vp 的易感家系相比,易感家系的肝胰腺中糖酵解、丝氨酸-甘氨酸代谢、嘌呤和嘧啶代谢水平较高,但甜菜碱-同型半胱氨酸代谢水平较低。有趣的是,Vp 感染诱导抗性家系中糖酵解、丝氨酸-甘氨酸代谢、嘌呤代谢、嘧啶代谢和磷酸戊糖途径上调,而甜菜碱-同型半胱氨酸代谢下调。此外,感染 Vp 后,抗性家系中的花生四烯酸代谢和一些免疫途径,如 NF-κB 和 cAMP 途径,上调。相反,在 Vp 感染后,易感家系通过 PEPCK 介导的 TCA 循环通量激活了氨基酸分解代谢。这些抗性家系和易感家系之间在转录组和代谢组上的差异可能有助于虾对细菌的抗性。重要的是,(Vp)是一种主要的水生病原体,可引起急性肝胰腺坏死病(AHPND),并导致对虾养殖业遭受巨大的经济损失。尽管最近发展了控制养殖环境的方法,但疾病抗性亲虾养殖仍然是水产疾病控制的一种可持续方法。在 Vp 感染期间发生了代谢变化,但对 AHPND 抗性的代谢知之甚少。转录组和代谢组的综合分析揭示了抗性和易感虾之间表现出的基础代谢差异。氨基酸分解代谢可能有助于 Vp 的发病机制,而花生四烯酸代谢可能是抗性表型的原因。这项研究将有助于阐明对虾对 AHPND 抗性的代谢和分子机制。此外,本研究中鉴定的氨基酸和花生四烯酸途径的关键基因和代谢物将应用于虾养殖产业的抗病性改良。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20ff/10469596/78d7d462f740/msystems.00067-23.f001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验