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Originally published In Press as doi:10.1074/jbc.M107599200 on September 19, 2001
J. Biol. Chem., Vol. 276, Issue 48, 44570-44574, November 30, 2001
Peroxisome Biogenesis and Selective Degradation Converge
at Pex14p*
Anna Rita
Bellu §,
Masayuki
Komori¶ ,
Ida J.
van der Klei **,
Jan A. K. W.
Kiel  , and
Marten
Veenhuis §§
From Eukaryotic Microbiology, Groningen Biomolecular
Sciences and Biotechnology Institute, University of Groningen, P. O. Box 14, 9750 AA Haren, The Netherlands and ¶ Laboratory
of Cellular and Molecular Biology, Department of Veterinary Science,
Graduate School of Agriculture and Biological Sciences, Osaka
Prefecture University, 1-1 Gakuen-cho, Sakai, Osaka 599-8531, Japan
We have analyzed the function of
Hansenula polymorpha Pex14p in selective peroxisome
degradation. Previously, we showed that Pex14p was involved in
peroxisome biogenesis and functions in peroxisome matrix protein
import. Evidence for the additional function of HpPex14p in selective
peroxisome degradation (pexophagy) came from cells defective in
HpPex14p synthesis. The suggestion that the absence of HpPex14p
interfered with pexophagy was further analyzed by mutational analysis.
These studies indicated that deletions at the C terminus of up to 124 amino acids of HpPex14p did not affect peroxisome degradation.
Conversely, short deletions of the N terminus (31 and 64 amino acids,
respectively) of the protein fully impaired pexophagy. Peroxisomes
present in these cells remained intact for at least 6 h of
incubation in the presence of excess glucose, conditions that led to
the rapid turnover of the organelles in wild-type control cells. We
conclude that the N terminus of HpPex14p contains essential information
to control pexophagy in H. polymorpha and thus, that
organelle development and turnover converge at Pex14p.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
§
Supported by an Erasmus grant.
Supported by grants-in-aid for scientific research from the
Ministry of Education, Culture, Sports, Science and Technology of Japan.
**
Holder of a PIONIER fellowship from Aard-en-Levenswetenschappen
(ALW), which is subsidized by the Dutch Organization for the Advancement of Pure Research.

Supported by a grant from ALW.
§§
To whom correspondence should be addressed. Tel.: 31-50-363-2176;
Fax: 31-50-363-8280; E-mail: M.Veenhuis@ biol.rug.nl.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.
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