{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T10:39:32Z","timestamp":1787567972233,"version":"build-2736575974"},"reference-count":58,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2024,12,10]],"date-time":"2024-12-10T00:00:00Z","timestamp":1733788800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2024,12,10]],"date-time":"2024-12-10T00:00:00Z","timestamp":1733788800000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2024,12,10]],"date-time":"2024-12-10T00:00:00Z","timestamp":1733788800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100010438","name":"Francis Crick Institute","doi-asserted-by":"publisher","award":["CC2132"],"award-info":[{"award-number":["CC2132"]}],"id":[{"id":"10.13039\/100010438","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["10.35802\/223192"],"award-info":[{"award-number":["10.35802\/223192"],"id":[{"id":"10.35802\/223192","id-type":"DOI","asserted-by":"publisher"}]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["TO 1349\/1-1"],"award-info":[{"award-number":["TO 1349\/1-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000265","name":"Medical Research Council","doi-asserted-by":"publisher","award":["MR\/V03314X\/1"],"award-info":[{"award-number":["MR\/V03314X\/1"]}],"id":[{"id":"10.13039\/501100000265","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["elifesciences.org"],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>\n                    <jats:italic>Toxoplasma gondii<\/jats:italic>\n                    is an intracellular parasite that subverts host cell functions via secreted virulence factors. Up to 70% of parasite-controlled changes in the host transcriptome rely on the MYR1 protein, which is required for the translocation of secreted proteins into the host cell. Mice infected with MYR1 knock-out (KO) strains survive infection, supporting a paramount function of MYR1-dependent secreted proteins in\n                    <jats:italic>Toxoplasma<\/jats:italic>\n                    virulence and proliferation. However, we have previously shown that MYR1 mutants have no growth defect in pooled\n                    <jats:italic>in vivo<\/jats:italic>\n                    CRISPR-Cas9 screens in mice, suggesting that the presence of parasites that are wild-type at the\n                    <jats:italic>myr1<\/jats:italic>\n                    locus in pooled screens can rescue the phenotype. Here, we demonstrate that MYR1 is not required for the survival in IFN-\u03b3-activated murine macrophages, and that parasites lacking MYR1 are able to expand during the onset of infection. While \u0394MYR1 parasites have restricted growth in single-strain murine infections, we show that the phenotype is rescued by co-infection with wild-type (WT) parasites\n                    <jats:italic>in vivo<\/jats:italic>\n                    , independent of host functional adaptive immunity or key pro-inflammatory cytokines. These data show that the major function of MYR1-dependent secreted proteins is not to protect the parasite from clearance within infected cells. Instead, MYR-dependent proteins generate a permissive niche in a paracrine manner, which rescues \u0394MYR1 parasites within a pool of CRISPR mutants in mice. Our results highlight an important limitation of otherwise powerful\n                    <jats:italic>in vivo<\/jats:italic>\n                    CRISPR screens and point towards key functions for MYR1-dependent\n                    <jats:italic>Toxoplasma<\/jats:italic>\n                    -host interactions beyond the infected cell.\n                  <\/jats:p>","DOI":"10.7554\/elife.102592","type":"journal-article","created":{"date-parts":[[2024,10,14]],"date-time":"2024-10-14T20:25:10Z","timestamp":1728937510000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.102592","source":"Crossref","is-referenced-by-count":0,"title":["Paracrine rescue of MYR1-deficient Toxoplasma gondii mutants reveals limitations of pooled in vivo CRISPR screens"],"prefix":"10.7554","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2299-9543","authenticated-orcid":true,"given":"Francesca","family":"Torelli","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04tnbqb63","id-type":"ROR","asserted-by":"publisher"}],"name":"Signalling in Apicomplexan Parasites Laboratory, The Francis Crick Institute","place":["London, United Kingdom"]},{"name":"Host-Pathogen Interactions Laboratory, Gulbenkian Institute for Molecular Medicine","place":["Oeiras, Portugal"]}],"role":[{"role":"author","vocabulary":"crossref"},{"role":"conceptualization","vocabulary":"credit"},{"role":"formal-analysis","vocabulary":"credit"},{"role":"investigation","vocabulary":"credit"},{"role":"methodology","vocabulary":"credit"},{"role":"visualization","vocabulary":"credit"},{"role":"writing-original-draft","vocabulary":"credit"},{"role":"writing-review-editing","vocabulary":"credit"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2796-6572","authenticated-orcid":true,"given":"Diogo M","family":"da Fonseca","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04tnbqb63","id-type":"ROR","asserted-by":"publisher"}],"name":"Signalling in Apicomplexan Parasites Laboratory, The Francis Crick Institute","place":["London, United Kingdom"]},{"name":"Host-Pathogen Interactions Laboratory, Gulbenkian Institute for Molecular Medicine","place":["Oeiras, 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