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PRMT1 is thought to be responsible for the majority of PRMT activity in\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma gondii<\/jats:named-content>\n                    , but its exact function is unknown. To further define the biological function of the PRMT family, we generated\n                    <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n                    mutants lacking PRMT1 (\u0394\n                    <jats:italic>prmt1<\/jats:italic>\n                    ) by deletion of the\n                    <jats:italic>PRMT1<\/jats:italic>\n                    gene. \u0394\n                    <jats:italic>prmt1<\/jats:italic>\n                    parasites exhibit morphological defects during cell division and grow slowly, and this phenotype reverses in the \u0394\n                    <jats:italic>prmt<\/jats:italic>\n                    ::\n                    <jats:italic>PRMT1mRFP<\/jats:italic>\n                    complemented strain. Tagged PRMT1 localizes primarily in the cytoplasm with enrichment at the pericentriolar material, and the strain lacking PRMT1 is unable to segregate progeny accurately. Unlike wild-type and complemented parasites, \u0394\n                    <jats:italic>prmt1<\/jats:italic>\n                    parasites have abnormal daughter buds, perturbed centrosome stoichiometry, and loss of synchronous replication. Whole-genome expression profiling demonstrated differences in expression of cell-cycle-regulated genes in the \u0394\n                    <jats:italic>prmt1<\/jats:italic>\n                    strain relative to the complemented \u0394\n                    <jats:italic>prmt1::PRMT1mRFP<\/jats:italic>\n                    and parental wild-type strains, but these changes do not correlate with a specific block in cell cycle. Although PRMT1\u2019s primary biological function was previously proposed to be methylation of histones, our studies suggest that PRMT1 plays an important role within the centrosome to ensure the proper replication of the parasite.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>IMPORTANCE<\/jats:bold>\n                    Apicomplexan parasites include several important pathogens, including\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma gondii<\/jats:named-content>\n                    , a major cause of opportunistic infections and congenital birth defects. These parasites divide using a unique form of cell division called endodyogeny that is different from those of most eukaryotes. PRMT1 is a conserved arginine methyltransferase that was thought to regulate gene expression of\n                    <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n                    by modifying histone methylation. Using genetic techniques, we show that disruption of PRMT1 affects the parasite\u2019s ability to perform accurate cell division. Our studies reveal an unexpected role for arginine methylation in centrosome biology and regulation of parasite replication.\n                  <\/jats:p>","DOI":"10.1128\/mbio.02094-15","type":"journal-article","created":{"date-parts":[[2016,2,2]],"date-time":"2016-02-02T21:03:28Z","timestamp":1454447008000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Toxoplasma gondii Arginine Methyltransferase 1 (PRMT1) Is Necessary for Centrosome Dynamics during Tachyzoite Cell Division"],"prefix":"10.1128","volume":"7","author":[{"given":"Kamal","family":"El Bissati","sequence":"first","affiliation":[{"name":"Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena S.","family":"Suvorova","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine, USF Health College of Medicine, University of South Florida, Tampa, Florida, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Xiao","sequence":"additional","affiliation":[{"name":"Laboratory for Macromolecular Analysis and Proteomics, Albert Einstein College of Medicine, Bronx, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Lucas","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine, USF Health College of Medicine, University of South Florida, Tampa, Florida, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajendra","family":"Upadhya","sequence":"additional","affiliation":[{"name":"Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanfen","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, 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