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CRISPR/Cas9 knockouts reveal genetic interaction between strain-transcendent erythrocyte determinants of Plasmodium falciparum invasion.
Kanjee, Usheer; Grüring, Christof; Chaand, Mudit; Lin, Kai-Min; Egan, Elizabeth; Manzo, Jale; Jones, Patrick L; Yu, Tiffany; Barker, Robert; Weekes, Michael P; Duraisingh, Manoj T.
Afiliación
  • Kanjee U; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
  • Grüring C; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
  • Chaand M; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
  • Lin KM; Cambridge Institute for Medical Research, Cambridge, CB2 OXY, United Kingdom.
  • Egan E; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
  • Manzo J; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
  • Jones PL; Sanofi-Genzyme, Waltham, MA 02451.
  • Yu T; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
  • Barker R; Sanofi-Genzyme, Waltham, MA 02451.
  • Weekes MP; Cambridge Institute for Medical Research, Cambridge, CB2 OXY, United Kingdom.
  • Duraisingh MT; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115; mduraisi@hsph.harvard.edu.
Proc Natl Acad Sci U S A ; 114(44): E9356-E9365, 2017 10 31.
Article en En | MEDLINE | ID: mdl-29078358
During malaria blood-stage infections, Plasmodium parasites interact with the RBC surface to enable invasion followed by intracellular proliferation. Critical factors involved in invasion have been identified using biochemical and genetic approaches including specific knockdowns of genes of interest from primary CD34+ hematopoietic stem cells (cRBCs). Here we report the development of a robust in vitro culture system to produce RBCs that allow the generation of gene knockouts via CRISPR/Cas9 using the immortal JK-1 erythroleukemia line. JK-1 cells spontaneously differentiate, generating cells at different stages of erythropoiesis, including terminally differentiated nucleated RBCs that we term "jkRBCs." A screen of small-molecule epigenetic regulators identified several bromodomain-specific inhibitors that promote differentiation and enable production of synchronous populations of jkRBCs. Global surface proteomic profiling revealed that jkRBCs express all known Pfalciparum host receptors in a similar fashion to cRBCs and that multiple Pfalciparum strains invade jkRBCs at comparable levels to cRBCs and RBCs. Using CRISPR/Cas9, we deleted two host factors, basigin (BSG) and CD44, for which no natural nulls exist. BSG interacts with the parasite ligand Rh5, a prominent vaccine candidate. A BSG knockout was completely refractory to parasite invasion in a strain-transcendent manner, confirming the essential role for BSG during invasion. CD44 was recently identified in an RNAi screen of blood group genes as a host factor for invasion, and we show that CD44 knockout results in strain-transcendent reduction in invasion. Furthermore, we demonstrate a functional interaction between these two determinants in mediating Pfalciparum erythrocyte invasion.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Plasmodium falciparum / Eritrocitos / Sistemas CRISPR-Cas Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Plasmodium falciparum / Eritrocitos / Sistemas CRISPR-Cas Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos