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Open Access item Vacuole membrane protein 1, autophagy and much more

Authors:Calvo-Garrido, Javier
Carilla-Latorre, Sergio
Escalante, Ricardo
Keywords:Vacuole membrane protein 1, Organelle biogenesis, Autophagy, Protein secretion, Osmoregulation, Dictyostelium, Endoplasmic reticulum
Issue Date:Aug-2008
Publisher:Landes Bioscience
Citation:Autophagy 16(4): 835-837 (2008)
Abstract:Vacuole membrane protein 1 (Vmp1) is a putative transmembrane protein that has been associated with different functions including autophagy, cell adhesion, and membrane traffic. Highly similar proteins are present in lower eukaryotes and plants although a homologue is absent in the fungi lineage. We have recently described the first loss-of-function mutation for a Vmp1 homologue in a model system, Dictyostelium discoideum. Our results give a more comprehensive view of the intricate roles played by this new gene. Dictyostelium Vmp1 is an endoplasmic reticulum-resident protein. Cells deficient in Vmp1 display pleiotropic defects in the context of the secretory pathway such as organelle biogenesis, the endocytic pathway, and protein secretion. The biogenesis of the contractile vacuole, an organelle necessary to survive under hypoosmotic conditions, is compromised as well as the structure of the endoplasmic reticulum and the Golgi apparatus. Transmission electron microscopy also shows abnormal accumulation of aberrant double-membrane vesicles, suggesting a defect in autophagosome biogenesis or maturation. The expression of a mammalian Vmp1 in the Dictyostelium mutant complements the phenotype suggesting a functional conservation during evolution. We are taking the first steps in understanding the function of this fascinating protein and recent studies have brought us more questions than answers about its basic function and its role in human pathology.
Description:3 pages, 2 figures, 1 table.-- Article addendum.-- This article is Open Access.
Publisher version (URL):http://www.landesbioscience.com/journals/autophagy/article/6574
Appears in Collections:(IIBM) Artículos

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