Acetylome analysis of the feline small intestine followingToxoplasma gondiiinfection

文献类型： 外文期刊

第一作者： Meng, Yu-Meng

作者： Meng, Yu-Meng;Zhao, Quan;Zhu, Xing-Quan;Meng, Yu-Meng;Zhai, Bin-Tao;Xie, Shi-Chen;Zhu, Xing-Quan;He, Jun-Jun;Elsheikha, Hany M.;Wang, Ze-Xiang;Zhu, Xing-Quan

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关键词： Toxoplasma gondii; Posttranslational modification; Cat; Lysine acetylation

期刊名称：PARASITOLOGY RESEARCH （ 影响因子：2.289； 五年影响因子：2.403 ）

ISSN： 0932-0113

年卷期： 2020 年 119 卷 11 期

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收录情况： SCI

摘要： Toxoplasma gondiiis a protozoan parasite capable of infecting a large number of warm-blooded animals and causes serious health complications in immunocompromised patients.T. gondiiinfection of the feline small intestine is critical for the completion of the life cycle and transmission ofT. gondii. Protein acetylation is an important posttranslational modification, which plays roles in the regulation of various cellular processes. Therefore, understanding of howT. gondiireprograms the protein acetylation status of feline definitive host can help to thwart the production and spread ofT. gondii. Here, we used affinity enrichment and high-resolution liquid chromatography with tandem mass spectrometry to profile the alterations of the acetylome in cat small intestine 10 days after infection byT. gondiiPrugniuad (Pru) strain. Our analysis showed thatT. gondiiinduced significant changes in the acetylation of proteins in the cat intestine. We identified 2606 unique lysine acetylation sites in 1357 acetylated proteins. The levels of 334 acetylated peptides were downregulated, while the levels of 82 acetylated peptides were increased in the infected small intestine. The proteins with differentially acetylated peptides were particularly enriched in the bioenergetics-related processes, such as tricarboxylic acid cycle, oxidative phosphorylation, and oxidation-reduction. These results provide the first baseline of the global acetylome of feline small intestine followingT. gondiiinfection and should facilitate further analysis of the role of acetylated protein in the pathogenesis ofT. gondiiinfection in its definitive host.

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