Comparative Analysis of Apicomplexa and Genomic Diversity in Eukaryotes
- Thomas J. Templeton1,7,8,
- Lakshminarayan M. Iyer2,7,
- Vivek Anantharaman2,
- Shinichiro Enomoto3,
- Juan E. Abrahante3,
- G.M. Subramanian5,
- Stephen L. Hoffman6,
- Mitchell S. Abrahamsen3,4, and
- L. Aravind2,8
- 1 Department of Microbiology and Immunology, Weill Medical College and the Program in Immunology and Microbial Pathogenesis, Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10021, USA
- 2 National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland 20894, USA
- 3 Department of Veterinary Pathobiology, University of Minnesota, St. Paul, Minnesota 55108, USA
- 4 Biomedical Genomics Center, University of Minnesota, St. Paul, Minnesota 55108, USA
- 5 Human Genome Sciences, Rockville, Maryland 20850, USA
- 6 Sanaria Inc., Rockville, Maryland 20852, USA
Abstract
The apicomplexans Plasmodium and Cryptosporidium have developed distinctive adaptations via lineage-specific gene loss and gene innovation in the process of diverging from a common parasitic ancestor. The two lineages have acquired distinct but overlapping sets of surface protein adhesion domains typical of animal proteins, but in no case do they share multidomain architectures identical to animals. Cryptosporidium, but not Plasmodium, possesses an animal-type O-linked glycosylation pathway, along with >30 predicted surface proteins having mucin-like segments. The two parasites have notable qualitative differences in conserved protein architectures associated with chromatin dynamics and transcription. Cryptosporidium shows considerable reduction in the number of introns and a concomitant loss of spliceosomal machinery components. We also describe additional molecular characteristics distinguishing Apicomplexa from other eukaryotes for which complete genome sequences are available.
Footnotes
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[Supplemental material is available online at www.genome.org.]
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Article and publication are at http://www.genome.org/cgi/doi/10.1101/gr.2615304.
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↵7 These authors contributed equally to this work.
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↵8 Corresponding authors. E-MAIL aravind{at}ncbi.nlm.nih.gov; FAX (301) 435-7794. E-MAIL tjt2001{at}med.cornell.edu; FAX (212) 746-4028.
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- Accepted June 14, 2004.
- Received March 23, 2004.
- Cold Spring Harbor Laboratory Press
