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J. Biol. Chem., Vol. 278, Issue 10, 8597-8605, March 7, 2003
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From the The mammalian dynamin-like protein 1 (DLP1), a
member of the dynamin family of large GTPases, possesses
mechanochemical properties known to constrict and tubulate membranes.
In this study, we have combined two experimental approaches, induction
of peroxisome proliferation by Pex11p
Dynamin-like Protein 1 Is Involved in
Peroxisomal Fission*
,
Department of Cell Biology and Cell
Pathology, University of Marburg, Robert Koch Str. 5, D-35037 Marburg,
Germany, the § Department of Anatomy and Cell Biology,
Division of Medical Cell Biology, University of Heidelberg, Im
Neuenheimer Feld 307, D-69120 Heidelberg, Germany, and the
¶ Department of Biochemistry and Molecular Biology, Mayo Clinic,
Rochester, Minnesota 55905
and expression of
dominant-negative mutants, to test whether DLP1 plays a role in
peroxisomal growth and division. We were able to localize DLP1 in spots
on tubular peroxisomes in HepG2 cells. In addition, immunoblot analysis
revealed the presence of DLP1 in highly purified peroxisomal fractions
from rat liver and an increase of DLP1 after treatment of rats with the
peroxisome proliferator bezafibrate. Expression of a dominant negative
DLP1 mutant deficient in GTP hydrolysis (K38A) either alone or in
combination with Pex11p caused the appearance of tubular peroxisomes
but had no influence on their intracellular distribution. In
co-expressing cells, the formation of tubulo-reticular networks of
peroxisomes was promoted, and peroxisomal division was completely
inhibited. These findings were confirmed by silencing of DLP1 using
siRNA. We propose a direct role for the dynamin-like protein DLP1 in
peroxisomal fission and in the maintenance of peroxisomal morphology in
mammalian cells.
*
This work was supported in part by a grant of the Medizin
Stiftung (Marburg, Germany) (to A. K.).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.
To whom correspondence should be addressed: Dept. of Cell
Biology and Cell Pathology, University of Marburg, Robert-Koch Str. 5, D-35037 Marburg, Germany. Tel.: 6421-28-63857; Fax: 6421-28-66414; E-mail: schrader@mailer.uni-marburg.de.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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