Integrated application of transcriptomics and metabolomics provides insights into acute hepatopancreatic necrosis disease resistance of Pacific white shrimp Litopenaeus vannamei.
Integrated application of transcriptomics and metabolomics provides insights into acute hepatopancreatic necrosis disease resistance of Pacific white shrimp Litopenaeus vannamei.
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DOI：
10.1128/msystems.00067-23
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发表时间：
2023-08-31
期刊：
影响因子：
6.4
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中科院分区：
文献类型：
--
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急性肝胰腺坏死病给对虾养殖业造成了巨大的经济损失。副溶血性弧菌（Vibrio parahaemolyticus，VpAHPND）是引起凡纳白色对虾AHPND的主要病原。然而，关于虾如何抵抗AHPND的知识非常有限。为了解对虾抗AHPND的分子机制，比较了对虾抗AHPND家系和感病家系的抗病性和抗病性。在转录和代谢水平上进行vannamei。对VpAHPND的靶组织--对虾肝胰腺的转录组学和代谢组学的综合分析表明，对虾的抗性家系与敏感家系之间存在显著差异。与未感染VpAHPND的抗性家系相比，易感家系肝胰腺糖酵解、丝氨酸-甘氨酸代谢、嘌呤和嘧啶代谢水平较高，而甜菜碱-同型半胱氨酸代谢水平较低。奇怪的是，在耐药家族中，VpAHPND感染诱导糖酵解、丝氨酸-甘氨酸代谢、嘌呤代谢、嘧啶代谢和磷酸戊糖途径的上调，以及甜菜碱-高半胱氨酸代谢的下调。此外，VpAHPND感染后，耐药家族花生四烯酸代谢及NF-κB、cAMP等免疫途径表达上调。与此相反，通过PEPCK介导的TCA循环通量增强的氨基酸催化剂在VpAHPND感染后的易感家族中被激活。抗性家系和敏感家系在转录组和代谢组上的差异可能是导致对虾对细菌抗性的原因之一。副溶血性弧菌（Vibrio parahaemolyticus，VpAHPND）是引起对虾急性肝胰腺坏死病（acute hepatopancreatic necrosis disease，AHPND）的主要病原菌，给对虾养殖业造成巨大的经济损失。尽管近年来养殖环境的控制取得了很大进展，但抗病亲鱼育种仍然是水产疾病控制的可持续途径。VpAHPND感染过程中发生代谢变化，但对AHPND抗性代谢的认识非常有限。转录组和代谢组的综合分析揭示了抗病虾和感病虾在基础代谢方面的差异。氨基酸代谢可能参与了VpAHPND的发病机制，花生四烯酸代谢可能是VpAHPND耐药表型的原因。本研究将有助于揭示对虾抗AHPND的代谢和分子机制。本研究所获得的氨基酸途径和花生四烯酸途径的关键基因及其代谢产物，将为对虾养殖业抗病性改良提供基础。
Acute hepatopancreatic necrosis disease (AHPND) has caused a huge economic loss to shrimp aquaculture. Vibrio parahaemolyticus (VpAHPND) is regarded as a major causative agent of AHPND in the Pacific white shrimp Litopenaeus vannamei. 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 L. vannamei were performed at transcriptional and metabolic levels. Integrated analysis of transcriptomics and metabolomics on hepatopancreas of shrimp, the target tissue of VpAHPND, 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 VpAHPND infection. Curiously, VpAHPND 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 VpAHPND infection. In contrast, amino acid catabolism boosted via PEPCK-mediated TCA cycle flux was activated in the susceptible family after VpAHPND infection. These differences in transcriptome and metabolome between resistant family and susceptible family might contribute to the resistance of shrimp to bacteria. Vibrio parahaemolyticus (VpAHPND) 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 VpAHPND 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 VpAHPND 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.
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影响因子：
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作者：
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DOI：
10.1073/pnas.1503129112
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影响因子：
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