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Eukaryotic Cell, January 2009, p. 19-26, Vol. 8, No. 1
1535-9778/09/$08.00+0 doi:10.1128/EC.00313-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

,2
Terrence D. Mulhern,2 and
Trevor Lithgow2,
School of Botany, University of Melbourne, Victoria 3010, Australia,1 Department of Biochemistry and Molecular Biology, Bio21 Institute of Biotechnology and Molecular Science, University of Melbourne, Victoria 3010, Australia2
Received 15 September 2008/ Accepted 8 November 2008
Microsporidia are a group of highly adapted obligate intracellular parasites that are now recognized as close relatives of fungi. Their adaptation to parasitism has resulted in broad and severe reduction at (i) a genomic level by extensive gene loss, gene compaction, and gene shortening; (ii) a biochemical level with the loss of much basic metabolism; and (iii) a cellular level, resulting in lost or cryptic organelles. Consistent with this trend, the mitochondrion is severely reduced, lacking ATP synthesis and other typical functions and apparently containing only a fraction of the proteins of canonical mitochondria. We have investigated the mitochondrial protein import apparatus of this reduced organelle in the microsporidian Encephalitozoon cuniculi and find evidence of reduced and modified machinery. Notably, a putative outer membrane receptor, Tom70, is reduced in length but maintains a conserved structure chiefly consisting of tetratricopeptide repeats. When expressed in Saccharomyces cerevisiae, EcTom70 inserts with the correct topology into the outer membrane of mitochondria but is unable to complement the growth defects of Tom70-deficient yeast. We have scanned genomic data using hidden Markov models for other homologues of import machinery proteins and find evidence of severe reduction of this system.
Published ahead of print on 21 November 2008.
Present address: Department of Biochemistry & Molecular Biology, Monash University, Victoria 3800, Australia.
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