1. Center for the Study of Biological Complexity, Virginia Commonwealth University, Richmond, Virginia 23284-2030, USA
2. Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia 23298-0678, USA
3. Philips Institute for Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond, Virginia 23298-0566, USA
4. Tufts University School of Veterinary Medicine, North Grafton, Massachusetts 01536, USA
5. Department of Microbiology, University of Virginia, Charlottesville, Virginia 22908, USA
6. Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22908, USA
7. MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK
8. Department of Biochemistry and Molecular Biophysics, Virginia Commonwealth University, Richmond, Virginia 23298-0614, USA
9. Department of Veterinary and Biomedical Sciences, University of Minnesota, St Paul, Minnesota 55108, USA
10. Biomedical Genomics Center, University of Minnesota, St Paul, Minnesota 55108, USA
11. Department of Microbiology, University of Minnesota, St Paul, Minnesota 55108, USA
12. These authors contributed equally to this work
13. Present address: Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA

Correspondence to: Gregory A. Buck^1,2 Email: buck@mail2.vcu.edu
Email: saul.tzipori@tufts.edu
The sequences reported in this paper have been deposited in GenBank under the project accession number AAEL000000. Further details of the accession numbers are available in the Supplementary Information.

Abstract

Cryptosporidium species cause acute gastroenteritis and diarrhoea worldwide. They are members of the Apicomplexa—protozoan pathogens that invade host cells by using a specialized apical complex and are usually transmitted by an invertebrate vector or intermediate host. In contrast to other Apicomplexans, Cryptosporidium is transmitted by ingestion of oocysts and completes its life cycle in a single host. No therapy is available, and control focuses on eliminating oocysts in water supplies¹. Two species, C. hominis and C. parvum, which differ in host range, genotype and pathogenicity, are most relevant to humans^{1, 2, 3}. C. hominis is restricted to humans, whereas C. parvum also infects other mammals². Here we describe the eight-chromosome 9.2-million-base genome of C. hominis². The complement of C. hominis protein-coding genes shows a striking concordance with the requirements imposed by the environmental niches the parasite inhabits. Energy metabolism is largely from glycolysis. Both aerobic and anaerobic metabolisms are available, the former requiring an alternative electron transport system in a simplified mitochondrion. Biosynthesis capabilities are limited, explaining an extensive array of transporters. Evidence of an apicoplast is absent, but genes associated with apical complex organelles are present. C. hominis and C. parvum exhibit very similar gene complements, and phenotypic differences between these parasites must be due to subtle sequence divergence.

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