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Identification and Characterization of a Novel Apical Membrane Antigen 3 in Eimeria tenella
Author(s) -
Wang Qingjie,
Zhu Shunhai,
Zhao Qiping,
Huang Bing,
Yu Shuilan,
Yu Yu,
Liang Shanshan,
Wang Haixia,
Zhao Huanzhi,
Han Hongyu,
Dong Hui
Publication year - 2021
Publication title -
journal of eukaryotic microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.067
H-Index - 77
eISSN - 1550-7408
pISSN - 1066-5234
DOI - 10.1111/jeu.12836
Subject(s) - biology , eimeria , apicomplexa , microneme , rhoptry , microbiology and biotechnology , intracellular parasite , coccidia , antigen , apical membrane , schizogony , parasite hosting , intracellular , plasmodium falciparum , genetics , immunology , epithelium , malaria , world wide web , computer science
Eimeria tenella is an obligate intracellular parasite in the phylum Apicomplexa. As described for other members of Apicomplexa, apical membrane antigen 1 (AMA1) has been shown to be critical for sporozoite invasion of host cells by E. tenella . Recently, an E. tenella paralogue of AMA1 (EtAMA1), dubbed sporoAMA1 (EtAMA3), was identified in proteomic and transcriptomic analyses of E. tenella , but not further characterized. Here, we show that EtAMA3 is a type I integral membrane protein that has 24% −38% identity with other EtAMAs. EtAMA3 has the same pattern of Cys residues in domains I and II of AMA1 orthologs from apicomplexan parasites, but high variance in domain III, with all six invariant Cys residues absent. EtAMA3 expression was developmentally regulated at the mRNA and protein levels. EtAMA3 protein was detected in sporulated oocysts and sporozoites, but not in the unsporulated oocysts or second‐generation merozoites. EtAMA3 is secreted by micronemes and is primarily localized to the apical end of sporozoites during host‐cell invasion. Additionally, pretreatment of sporozoites with rEtAMA3‐specific antibodies substantially impeded their invasion into host cells. These results suggest EtAMA3 is a sporozoite‐specific protein that is involved in host‐cell sporozoite invasion.