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对感染对虾虹彩病毒(EHP)的凡纳滨对虾(Penaeus vannamei)肠道和肝胰腺的转录组分析。

Transcriptome analysis of pacific white shrimp (Penaeus vannamei) intestines and hepatopancreas in response to Enterocytozoon hepatopenaei (EHP) infection.

机构信息

Key Laboratory of East China Sea Fishery Resources Exploitation, Ministry of Agriculture, East China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Shanghai 200090, China.

Key Laboratory of East China Sea Fishery Resources Exploitation, Ministry of Agriculture, East China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Shanghai 200090, China; Guangdong Provincial Key Laboratory of Marine Biotechnology, Shantou University, Shantou 515063, China.

出版信息

J Invertebr Pathol. 2021 Nov;186:107665. doi: 10.1016/j.jip.2021.107665. Epub 2021 Sep 11.

Abstract

Penaeus vannamei is the most economically important species of shrimp cultured worldwide. Enterocytozoon hepatopenaei (EHP) is an emerging pathogen that severely affects the growth and development of shrimps. In this study, the transcriptome differences between EHP-infected and uninfected shrimp were investigated through next-generation sequencing. The unigenes were assembled with the reads from all the four libraries. The differentially expressed genes (DEGs) of intestines and hepatopancreas were analyzed. There were 2,884 DEGs in the intestines and 2,096 DEGs in the hepatopancreas. The GO and KEGG enrichment analysis indicated that DEGs were significantly enriched in signaling pathways associated with nutritional energy metabolism and mobilizing autoimmunity. Moreover, the results suggested the downregulation of key genes in energy synthesis pathways contributed greatly to shrimp growth retardation; the upregulation of immune-related genes enhanced the resistance of shrimp against EHP infection. This study provided identified genes and pathways associated with EHP infection revealing the molecular mechanisms of growth retardation.

摘要

凡纳滨对虾是世界上最重要的经济虾类养殖品种。肝肠胞虫(EHP)是一种新兴的病原体,严重影响虾的生长和发育。在这项研究中,通过下一代测序技术研究了 EHP 感染和未感染虾之间的转录组差异。使用来自所有四个文库的读取内容对 unigenes 进行了组装。分析了肠和肝胰腺的差异表达基因(DEGs)。肠中有 2884 个 DEGs,肝胰腺中有 2096 个 DEGs。GO 和 KEGG 富集分析表明,DEGs 显著富集在与营养能量代谢和动员自身免疫相关的信号通路中。此外,结果表明,能量合成途径关键基因的下调极大地促进了虾的生长迟缓;免疫相关基因的上调增强了虾对 EHP 感染的抵抗力。本研究提供了与 EHP 感染相关的鉴定基因和途径,揭示了生长迟缓的分子机制。

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