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Molecular and Cellular Biology, October 2000, p. 7220-7229, Vol. 20, No. 19
Institute of Biochemistry and
Biophysics, 02-106 Warsaw,1 and Faculty
of Biotechnology, University of Gdansk, 80-822 Gdansk,3 Poland; Biozentrum, University
of Basel, CH-4056 Basel, Switzerland2;
and MPI Enzymology of Protein Folding, Biozentrum Halle,
D-06120 Halle, Germany4
Received 15 May 2000/Accepted 29 June 2000
Nam9p is a protein of the mitochondrial ribosome. The
respiration-deficient Saccharomyces cerevisiae strain
MB43-nam9-1 expresses Nam9-1p containing the point mutation
S82L. Respiratory deficiency correlates with a decrease in the steady
level of some mitochondrially encoded proteins and the complete lack of
mitochondrially encoded cytochrome oxidase subunit 2 (Cox2). De novo
synthesis of Cox2 in MB43-nam9-1 is unaffected, indicating
that newly synthesized Cox2 is rapidly degraded. Respiratory deficiency
of MB43-nam9-1 is overcome by transient overexpression of
HSP104, by deletion of HSP104, by transient
exposure to guanidine hydrochloride, and by expression of the
C-terminal portion of Sup35, indicating an involvement of the yeast
prion [PSI+]. Respiratory deficiency of
MB43-nam9-1 can be reinduced by transfer of cytosol from
S. cerevisiae that harbors
[PSI+]. We conclude that nam9-1
causes respiratory deficiency only in combination with the cytosolic
prion [PSI+], presenting the first example of
a synthetic effect between cytosolic [PSI+]
and a mutant mitochondrial protein.
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Prion-Dependent Switching between Respiratory
Competence and Deficiency in the Yeast nam9-1
Mutant
*
Corresponding author. Mailing address: MPI Enzymology
of Protein Folding, Biozentrum Halle, Weinbergweg 22, D-06120 Halle, Germany. Phone: 49-345-5522830. Fax: 49-345-5511972. E-mail for Sabine Rospert: rospert{at}enzyme-halle.mpg.de. E-mail for
Magdalena Boguta: magda{at}ibbrain.ibb.waw.pl.
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