{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T06:27:35Z","timestamp":1791354455894,"version":"4.3.1"},"reference-count":38,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2014,10,1]],"date-time":"2014-10-01T00:00:00Z","timestamp":1412121600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The obligate intracellular parasite\n            <jats:named-content content-type=\"genus-species\">Toxoplasma gondii<\/jats:named-content>\n            critically relies on host cell invasion during infection. Proteins secreted from the apical micronemes are central components for host cell recognition, invasion, egress, and virulence. Although previous work established that the sporozoite protein with an altered thrombospondin repeat (SPATR) is a micronemal protein conserved in other apicomplexan parasites, including\n            <jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>\n            ,\n            <jats:named-content content-type=\"genus-species\">Neospora<\/jats:named-content>\n            , and\n            <jats:named-content content-type=\"genus-species\">Eimeria<\/jats:named-content>\n            , no genetic evidence of its contribution to invasion has been reported. SPATR contains a predicted epidermal growth factor domain and two thrombospondin type 1 repeats, implying a role in host cell recognition. In this study, we assess the contribution of\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            SPATR (TgSPATR) to\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            invasion by genetically ablating it and restoring its expression by genetic complementation. \u0394\n            <jats:italic>spatr<\/jats:italic>\n            parasites were \u223c50% reduced in invasion compared to parental strains, a defect that was reversed in the complemented strain. In mouse virulence assays, \u0394\n            <jats:italic>spatr<\/jats:italic>\n            parasites were significantly attenuated, with \u223c20% of mice surviving infection. Given the conservation of this protein among the Apicomplexa, we assessed whether the\n            <jats:named-content content-type=\"genus-species\">Plasmodium falciparum<\/jats:named-content>\n            SPATR ortholog (PfSPATR) could complement the absence of the TgSPATR. Although PfSPATR showed correct micronemal localization, it did not reverse the invasion deficiency of \u0394\n            <jats:italic>spatr<\/jats:italic>\n            parasites, because of an apparent failure in secretion. Overall, the results suggest that TgSPATR contributes to invasion and virulence, findings that have implications for the many genera and life stages of apicomplexans that express SPATR.\n          <\/jats:p>","DOI":"10.1128\/iai.01877-14","type":"journal-article","created":{"date-parts":[[2014,8,5]],"date-time":"2014-08-05T03:38:42Z","timestamp":1407209922000},"page":"4358-4368","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":45,"title":["A Conserved Apicomplexan Microneme Protein Contributes to Toxoplasma gondii Invasion and Virulence"],"prefix":"10.1128","volume":"82","author":[{"given":"My-Hang","family":"Huynh","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin J.","family":"Boulanger","sequence":"additional","affiliation":[{"name":"Department of Biochemistry &amp; Microbiology, University of Victoria, Victoria, British Columbia, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vern B.","family":"Carruthers","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(04)16412-X"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.05013-11"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2011.01597.x"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2011.01585.x"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mib.2006.06.017"},{"key":"e_1_3_3_7_2","first-page":"114","article-title":"Sequential protein secretion from three distinct organelles of Toxoplasma gondii accompanies invasion of human fibroblasts","volume":"73","author":"Carruthers VB","year":"1997","unstructured":"CarruthersVB SibleyLD. 1997. 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