Avian pathogenic Escherichia coli T6SS effector protein Hcp2a causes mitochondrial dysfunction through interaction with LETM1 protein in DF-1 cells

效应器 大肠杆菌 化学 致病性大肠杆菌 微生物学 生物 VI型分泌系统 生物化学 毒力 基因
作者
Lijuan Lu,Qi Zhao,Zhe Chen,Haiyang Wang,Xiao Wei,Bingyu Zhao,Zhenyu Wang,Ying Shao,Jing Tu,Xiangjun Song
出处
期刊:Poultry Science [Elsevier]
卷期号:: 103514-103514
标识
DOI:10.1016/j.psj.2024.103514
摘要

The type VI secretion system (T6SS) of avian pathogenic Escherichia coli (APEC) can affect the functions of eukaryotic cells by secreting or injecting effectors. Hemolysin co-regulatory protein (Hcp), one of the markers of the T6SS, is both a structural protein and an effector protein of the T6SS. According to previous studies, mitochondria in eukaryotic cells are targeted by pathogenic bacteria. However, little is known about the regulation of mitochondria in eukaryotic host cells by the T6SS effector protein Hcp of APEC. In our study, DF-1 cells co-incubated with Hcp2a protein for 6 h showed decreased mitochondrial membrane potential, increased Ca2+ concentration, and increased cellular reactive oxygen species (ROS) levels. We therefore conclude that Hcp2a protein causes dysfunction to mitochondria in DF-1 cells. To explain the mechanism that causes mitochondrial dysfunction, we reanalyzed the Hcp2a interaction protein dataset in DF-1 cells, and the Leucine zipper EF-hand-containing transmembrane protein 1 (LETM1), which is associated with mitochondria, was screened. The protein and molecular docking results showed that Hcp2a protein and LETM1 protein have better binding. Finally, subcellular localization results showed that Hcp2a was localized to mitochondria. In summary, Hcp2a effector proteins caused dysfunction to DF-1 cellular mitochondria, and we hypothesize that the interaction of Hcp2a protein with LETM1 protein induces mitochondrial dysfunction and promotes mitochondrial localization of Hcp2a in DF-1 cells.
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