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Genome of deadly amoeba shows surprising complexity, evidence of lateral gene transfer

The genome sequence of the parasitic amoeba Entamoeba histolytica, a leading cause of severe diarrheal disease in developing countries, includes an unexpectedly complex repertoire of sensory genes as well as a variety of bacterial-like genes that contribute to the organism's unique biology.

The report, which appears in the February 24 issue of Nature, presents the first genome-wide study of an amoeba. It is also the first genome sequence to be published from this class of amitochondrial human pathogens.

The analysis reveals the degradation of the E. histolytica genome in its transition from a free-living organism into a parasite of the human gut. At the same time, scientists also cataloged the retention and expansion of some gene families characteristic of more complex organisms.

Detailing the first systematic study of relatively recent horizontal gene transfer into a protist, scientists report evidence in the DNA sequence that E. histolytica likely picked up a significant number of its metabolic genes from bacterial co-inhabitants of the human gut. Identification of these genes sheds new light on the unusual shared biology between the parasitic amoeba and anaerobic gut bacteria.

The E. histolytica genome sequence is expected to help in the development of new vaccines as well as diagnostic tests that can distinguish the amoeba's most deadly strains. The parasite infects an estimated 50 million people and causes as many as 100,000 deaths a year -- second only to malaria as a cause of morbidity and mortality from a protist. The disease caused by E. histolytica is called amebiasis.

The sequencing of E. histolytica was a collaborative effort led by The Institute for Genomic Research (TIGR) in Rockville, MD, and by the Wellcome Trust Sanger Institute in the U.K. The project was supported by grants from the National Institute of Allergy and Infectious Diseases (NIAID), which is part of the National Institutes of Health, and from the
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Source:The Institute for Genomic Research


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