[1] Department of Cell Biology and Neuroscience, University of California Riverside, Riverside, CA 92521, USA
[2] Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA
[3] Centre for Computational Biology, Mines ParisTech, Fontainebleau, F-77300 France
[4] Institut Curie, Paris, F-75248, France
[5] U900, INSERM, Paris, F-75248, France
[6] Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA
[7] Shoklo Malaria Research Unit, Mae Sot, Tak, 63110, Thailand
[8] Mahidol Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand
[9] Department of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA
[10] School of Life Sciences, Queens Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK
[11] Department of Medical Parasitology and Infection Biology, Swiss Tropical and Public Health Institute, Basel 4051, Switzerland
[12] Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford, OX3 7FZ UK
[13] La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA
[14]Department of Computer Science and Engineering, University of Washington, Seattle, WA 98195, USA
[$] These authors contributed equally to this study
[#] Current address: Department of Microbiology, Immunology and Molecular Genetics, UT Health San Antonio, San Antonio, TX 78229, USA
[*] Communicating authors:
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The development of malaria parasites throughout their various life cycle stages is controlled by coordinated changes in gene expression. We previously showed that the three-dimensional organization of the P. falciparum genome is strongly associated with gene expression during its replication cycle inside red blood cells. Here, we analyzed genome organization in the P. falciparum and P. vivax transmission stages. Major changes occurred in the localization and interactions of genes involved in pathogenesis and immune evasion, erythrocyte and liver cell invasion, sexual differentiation and master regulation of gene expression. In addition, we observed reorganization of subtelomeric heterochromatin around genes involved in host cell remodeling. Depletion of heterochromatin protein 1 (PfHP1) resulted in loss of interactions between virulence genes, confirming that PfHP1 is essential for maintenance of the repressive center. Overall, our results suggest that the three-dimensional genome structure is strongly connected with transcriptional activity of specific gene families throughout the life cycle of human malaria parasites.