Identification of multiple ferritin genes in Macrobrachium nipponense and their involvement in redox homeostasis and innate immunity.

Identification of multiple ferritin genes in Macrobrachium nipponense and their involvement in redox homeostasis and innate immunity.
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日本沼虾中多个铁蛋白基因的鉴定及其与氧化还原稳态和先天免疫的关系。

DOI:
10.1016/j.fsi.2019.04.050
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发表时间:
2019
期刊:
Fish Shellfish Immunol
影响因子:
--
通讯作者:
Liu Fengsong
Liu Fengsong
中科院分区:
其他
文献类型:
--
作者:
Tang Ting;Yang Zilan;Li Jing;Yuan Fengyu;Xie Song;Liu Fengsong

文献摘要

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基于转录组数据库,我们从日本沼虾中筛选出4个铁蛋白亚基基因(MnFer2-5),编码2个非分泌性多肽和2个分泌性多肽。MnFe2和4具有严格保守的铁氧酶活性中心,而MnFe3具有非典型的铁氧基活性中心。MnFer5似乎是一些铁蛋白家族,具有明显的双核金属结合基序,但缺乏铁离子通道、铁氧合酶和成核位点。这四个基因的不同组织特异性转录表明它们在对虾中的功能多样性。其中,MnFe_2主要在肝胰腺和肠道中表达,MnFe_3和MnFe_4主要在鳃中表达,而MnFe_5在各种组织中广泛表达,在肠道、肝胰腺和血细胞中高表达。所有四个MnFer基因的转录都能被阿霉素强烈诱导,这表明这些铁蛋白亚基参与了对氧化应激的保护。在嗜水气单胞菌感染过程中,只有MnFe5持续上调,而包括MnFe2-4在内的其他亚基在细菌攻击早期表达下调,随后恢复,甚至在细菌攻击后48 h略有增加。此外,体外实验还证实了重组MnFe2的铁结合能力。就是你。在大肠杆菌中表达的MnFe2表现出对过氧化氢酶细胞毒性的增强抗性。这些结果表明,弗洛姆铁素具有保护作用。日本血凝素铁稳态、氧化还原生物学和抗菌免疫,并阐明甲壳类铁蛋白亚基的分子进化。
Based on the transcriptome database, we screened out four ferritin subunit genes (MnFer2-5) from the oriental river prawn Macrobrachium nipponense, which encode two non-secretory and two secretory peptides. MnFer2 and 4 possess a strictly conserved ferroxidase site, and MnFer3 has a non-typical ferroxidase site. MnFer5 seems to be a number of ferritin families, which has a distinct dinuclear metal binding motif, but lacks an iron ion channel, a ferroxidase site and a nucleation site. Diverse tissue-specific transcriptions of the four genes indicate their functional diversity in the prawn. Among them, MnFer2 is mainly expressed in hepatopancreas and intestines, MnFer3 and 4 are predominantly expressed in gills, and MnFer5 is widely expressed in various tissues with high presence in intestines, hepatopancreas and haemocytes. The transcription of all the four MnFer genes can be strongly induced by doxorubicin, indicating the involvement of these ferritin subunits in protection from oxidative stress. Upon Aeromonas hydrophila infection, only MnFer5 is persistently up-regulated, while other subunits including MnFer2-4 are down-regulated during the early stage, followed by recovery and even a slight increase at 48 h post bacterial challenge. Moreover, the iron binding capacity of recombinant MnFer2 is also demonstrated in vitro. TheE. coliexpressing MnFer2 displays increased resistance to hydrogen peroxidase cytotoxicity. These results suggest a protective role of ferritins fromM. nipponensein iron homeostasis, redox biology and antibacterial immunity and shed light on the molecule evolution of crustacean ferritin subunits.