{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T08:04:04Z","timestamp":1792224244111,"version":"4.4.0"},"reference-count":53,"publisher":"National Academy of Sciences","issue":"23","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,6,4]]},"abstract":"<jats:p>\n                    Because parasite virulence factors target host immune responses, identification and functional characterization of these factors can provide insight into poorly understood host immune mechanisms. The fruit fly\n                    <jats:italic>Drosophila melanogaster<\/jats:italic>\n                    is a model system for understanding humoral innate immunity, but\n                    <jats:italic>Drosophila<\/jats:italic>\n                    cellular innate immune responses remain incompletely characterized. Fruit flies are regularly infected by parasitoid wasps in nature and, following infection, flies mount a cellular immune response culminating in the cellular encapsulation of the wasp egg. The mechanistic basis of this response is largely unknown, but wasps use a mixture of virulence proteins derived from the venom gland to suppress cellular encapsulation. To gain insight into the mechanisms underlying wasp virulence and fly cellular immunity, we used a joint transcriptomic\/proteomic approach to identify venom genes from\n                    <jats:italic>Ganaspis sp.1<\/jats:italic>\n                    (G1), a previously uncharacterized\n                    <jats:italic>Drosophila<\/jats:italic>\n                    parasitoid species, and found that G1 venom contains a highly abundant sarco\/endoplasmic reticulum calcium ATPase (SERCA) pump. Accordingly, we found that fly immune cells termed plasmatocytes normally undergo a cytoplasmic calcium burst following infection, and that this calcium burst is required for activation of the cellular immune response. We further found that the plasmatocyte calcium burst is suppressed by G1 venom in a SERCA-dependent manner, leading to the failure of plasmatocytes to become activated and migrate toward G1 eggs. Finally, by genetically manipulating plasmatocyte calcium levels, we were able to alter fly immune success against G1 and other parasitoid species. Our characterization of parasitoid wasp venom proteins led us to identify plasmatocyte cytoplasmic calcium bursts as an important aspect of fly cellular immunity.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1222351110","type":"journal-article","created":{"date-parts":[[2013,5,21]],"date-time":"2013-05-21T01:03:59Z","timestamp":1369098239000},"page":"9427-9432","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":96,"title":["Parasitoid wasp venom SERCA regulates\n                    <i>Drosophila<\/i>\n                    calcium levels and inhibits cellular immunity"],"prefix":"10.1073","volume":"110","author":[{"given":"Nathan T.","family":"Mortimer","sequence":"first","affiliation":[{"name":"Departments of aBiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy","family":"Goecks","sequence":"additional","affiliation":[{"name":"Departments of aBiology and"},{"name":"Mathematics and Computer Science, Emory University, Atlanta, GA 30322; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Balint Z.","family":"Kacsoh","sequence":"additional","affiliation":[{"name":"Departments of aBiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James A.","family":"Mobley","sequence":"additional","affiliation":[{"name":"Department of Surgery and"},{"name":"Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory J.","family":"Bowersock","sequence":"additional","affiliation":[{"name":"Department of Surgery and"},{"name":"Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Taylor","sequence":"additional","affiliation":[{"name":"Departments of aBiology and"},{"name":"Mathematics and Computer Science, Emory University, Atlanta, GA 30322; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Todd A.","family":"Schlenke","sequence":"additional","affiliation":[{"name":"Departments of aBiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2013,5,20]]},"reference":[{"key":"e_1_3_4_1_2","doi-asserted-by":"crossref","first-page":"S29","DOI":"10.1017\/S0031182000084924","article-title":"The coevolution of host resistance and parasitoid virulence","volume":"116","author":"Kraaijeveld AR","year":"1998","unstructured":"AR Kraaijeveld, JJ Van Alphen, HC Godfray, The coevolution of host resistance and parasitoid virulence. 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