Relationship between Protein kinase C and derepression of different enzymes.
Nenhuma Miniatura Disponível
Data
2002
Título da Revista
ISSN da Revista
Título de Volume
Editor
Resumo
The PKC1 gene in the yeast Saccharomyces cerevisiae
encodes for protein kinase C which is known to control a
MAP kinase cascade consisting of di¡erent kinases: Bck1,
Mkk1 and Mkk2, and Mpk1. This cascade a¡ects the cell
wall integrity but the phenotype of pkc1v mutants suggests
additional targets that have not yet been identi¢ed [Heinisch
et al., Mol. Microbiol. 32 (1999) 671^680]. The pkc1v mutant,
as opposed to other mutants in the MAP kinase cascade, displays
defects in the control of carbon metabolism. One of them
occurs in the derepression of SUC2 gene after exhaustion of
glucose from the medium, suggesting an involvement of Pkc1p
in the derepression process that is not shared by the downstream
MAP kinase cascade. In this work, we demonstrate that Pkc1p
is required for the increase of the activity of enzymatic systems
during the derepression process. We observed that Pkc1p is
involved in the derepression of invertase and alcohol dehydrogenase
activities. On the other hand, it seems not to be necessary
for the derepression of the enzymes of the GAL system. Our
results suggest that Pkc1p is acting through the main glucose
repression pathway, since introduction of an additional mutation
in the PKC1 gene in yeast strains already presenting mutations
in the HXKII or MIG1 genes does not interfere with the typical
derepressed phenotype observed in these single mutants. Moreover,
our data indicate that Pkc1p participates in this process
through the control of the cellular localization of the Mig1
transcriptional factor.
Descrição
Palavras-chave
Saccharomyces cerevisiae, Signal transduction
Citação
SALGADO, A. P. C. et al. Relationship between protein kinase C and derepression of different enzymes. Febs Letters, v. 532, p.324-332, 2002. Disponível em: <http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(02)03695-5/epdf>. Acesso em: 10 jan. 2017.