Mutation of a putative AMPK phosphorylation site abolishes the repressor activity but not the nuclear targeting of the fungal glucose regulator CRE1

Citation
G. Vautard-mey et M. Fevre, Mutation of a putative AMPK phosphorylation site abolishes the repressor activity but not the nuclear targeting of the fungal glucose regulator CRE1, CURR GENET, 37(5), 2000, pp. 328-332
Citations number
29
Categorie Soggetti
Molecular Biology & Genetics
Journal title
CURRENT GENETICS
ISSN journal
01728083 → ACNP
Volume
37
Issue
5
Year of publication
2000
Pages
328 - 332
Database
ISI
SICI code
0172-8083(200005)37:5<328:MOAPAP>2.0.ZU;2-C
Abstract
In filamentous ascomycetes, glucose repression is mediated by CRE1, a zinc- finger protein related to Mig1p from yeast. Five putative AMPK phosphorylat ion motifs identified ill the glucose repressor from the phytopathogenic fu ngus Sclerotinia sclerotiorum were mutated in a GFP::CRE1 translational fus ion. Complementation experiments in Aspergillus nidulans and fluorescence m icroscopy analyses showed that mutation of one site (Ser(266)) abolishes th e repressor activity of the fusion protein but not its nuclear targeting, s uggesting that an AMPK protein kinase may be involved in the function of th e fungal glucose repressor.