{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T21:30:40Z","timestamp":1792704640738,"version":"4.5.0"},"reference-count":173,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2014,9,1]],"date-time":"2014-09-01T00:00:00Z","timestamp":1409529600000},"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":["Microbiol Mol Biol Rev"],"published-print":{"date-parts":[[2014,9]]},"abstract":"<jats:title>SUMMARY<\/jats:title>\n          <jats:p>\n            Research into the complex genetic underpinnings of the malaria parasite\n            <jats:named-content content-type=\"genus-species\">Plasmodium falciparum<\/jats:named-content>\n            is entering a new era with the arrival of site-specific genome engineering. Previously restricted only to model systems but now expanded to most laboratory organisms, and even to humans for experimental gene therapy studies, this technology allows researchers to rapidly generate previously unattainable genetic modifications. This technological advance is dependent on DNA double-strand break repair (DSBR), specifically homologous recombination in the case of\n            <jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>\n            . Our understanding of DSBR in malaria parasites, however, is based largely on assumptions and knowledge taken from other model systems, which do not always hold true in\n            <jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>\n            . Here we describe the causes of double-strand breaks, the mechanisms of DSBR, and the differences between model systems and\n            <jats:named-content content-type=\"genus-species\">P. falciparum<\/jats:named-content>\n            . These mechanisms drive basic parasite functions, such as meiosis, antigen diversification, and copy number variation, and allow the parasite to continually evolve in the contexts of host immune pressure and drug selection. Finally, we discuss the new technologies that leverage DSBR mechanisms to accelerate genetic investigations into this global infectious pathogen.\n          <\/jats:p>","DOI":"10.1128\/mmbr.00059-13","type":"journal-article","created":{"date-parts":[[2014,9,2]],"date-time":"2014-09-02T20:37:01Z","timestamp":1409690221000},"page":"469-486","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":116,"title":["DNA Repair Mechanisms and Their Biological Roles in the Malaria Parasite Plasmodium falciparum"],"prefix":"10.1128","volume":"78","author":[{"given":"Andrew H.","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Columbia University, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lorraine S.","family":"Symington","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Columbia University, New York, 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