Formation of multivesicular endosomes in Dictyostelium.

Abstract:

:Multivesicular endosomes are present in virtually every eucaryotic cell, where they arise by intra-endosomal budding of the limiting endosomal membrane. Some genetic diseases such as Chediak-Higashi syndrome are characterized by enlarged membrane-filled endosomes. The same altered endosomal morphology can be observed in cells exposed to certain drugs, for example U18666A. The mechanisms involved are still poorly characterized, partially because this atypical budding event is particularly difficult to observe in mammalian cells. Taking advantage of the simplicity of the endosomal structure in Dictyostelium discoideum, we could visualize intraendosomal budding at the ultrastructural level. In this model organism, the drug U18666A was shown to stimulate intra-endosomal budding, while an inhibitor of PI 3-kinase activity was found to have no effect on this process. Inactivation of a Dictyostelium gene with similarity to the gene responsible for Chediak-Higashi syndrome did not alter the intra-endosomal budding or the accumulation of intra-endosomal membranes. Thus, although treatment with U18666A and inactivation of the Chediak-Higashi gene cause similar morphological defects in mammalian cells, observations in a different model reveal that their respective modes of action are different.

journal_name

J Cell Sci

journal_title

Journal of cell science

authors

Marchetti A,Mercanti V,Cornillon S,Alibaud L,Charette SJ,Cosson P

doi

10.1242/jcs.01524

keywords:

subject

Has Abstract

pub_date

2004-12-01 00:00:00

pages

6053-9

issue

Pt 25

eissn

0021-9533

issn

1477-9137

pii

jcs.01524

journal_volume

117

pub_type

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