Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/1716

TitleFps1p channel is the mediator of the major part of glycerol passive diffusion in Saccharomyces cerevisiae : artefacts and re-definitions
Author(s)Oliveira, Rui Pedro Soares de
Lages, Fernanda
Graça, Magda Maria Couto da Silva
Lucas, Cândida
KeywordsSaccharomyces cerevisiae
Glycerol transport/permeability artefact
FPS1
YFL 054c
GUT1
GUT2
S. cerevisiae
Issue date2003
PublisherElsevier
JournalBiochimica et Biophysica Acta (BBA). Biomembranes
Citation“Biochimica et biophysica acta”. 1613 (2003) 67-71.
Abstract(s)Glycerol has been shown to cross Saccharomyces cerevisiae plasma membrane (1) through a H+/symport detected in cells grown on non-fermentable carbon sources, (2) by passive diffusion and (3) through the constitutive Fps1p channel. This has been named a facilitator, for mediating glycerol low affinity transport of the facilitated diffusion type. We present experimental evidence that this kinetics is an artefact created by glycerol kinase activity. Instead, the channel is shown to mediate the major part of glycerol passive diffusion. Nevertheless, Fps1p major role in vivo has been previously shown to be the control of glycerol export under osmotic stress or in reaction to turgor changes. Overexpressing FPS1 caused an increase in H+/symport V_max. Moreover, yfl054c and fps1 mutants were equally affected by exogenously added ethanol, being the correspondent passive diffusion stimulated. This is, to our knowledge, the first time that a phenotype can be attributed to the functioning of YFL054c gene. Glycerol passive diffusion is thus apparently channel mediated. This is discussed according to glycerol chemical properties, which contradict the widely spread concept of glycerol lipossoluble nature. The discussion considers the multiple roles that glycerol intracellular levels and its pathway regulation might play as a central key to metabolism control.
TypeArticle
URIhttp://hdl.handle.net/1822/1716
DOI10.1016/S0005-2736(03)00138-X
ISSN0005-2736
Peer-Reviewedyes
AccessOpen access
Appears in Collections:DBio - Artigos/Papers

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