Nucleic Acids Research, Vol 25, Issue 18 3657-3664, Copyright © 1997 by Oxford University Press
J Dong and RC Dickson
Expression of the lactose-galactose regulon in Kluyveromyces lactis is
induced by lactose or galactose and repressed by glucose. Some components
of the induction and glucose repression pathways have been identified but
many remain unknown. We examined the role of the SNF1 (KlSNF1) and MIG1
(KlMIG1) genes in the induction and repression pathways. Our data show that
full induction of the regulon requires SNF1; partial induction occurs in a
Klsnf1 -deleted strain, indicating that a KlSNF1 -independent pathway(s)
also regulates induction. MIG1 is required for full glucose repression of
the regulon, but there must be a KlMIG1 -independent repression pathway
also. The KlMig1 protein appears to act downstream of the KlSnf1 protein in
the glucose repression pathway. Most importantly, the KlSnf1-KIMig
repression pathway operates by modulating KlGAL1 expression. Regulating
KlGAL1 expression in this manner enables the cell to switch the regulon off
in the presence of glucose. Overall, our data show that, while the Snf1 and
Mig1 proteins play similar roles in regulating the galactose regulon in
Saccharomyces cerevisiae and K.lactis , the way in which these proteins are
integrated into the regulatory circuits are unique to each regulon, as is
the degree to which each regulon is controlled by the two proteins.
ARTICLES
Glucose represses the lactose-galactose regulon in Kluyveromyces lactis through a SNF1 and MIG1- dependent pathway that modulates galactokinase (GAL1) gene expression
Department of Biochemistry and the L. P. Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY 40536-0084, USA.
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