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Titolo:
Transcriptional autoregulation and inhibition of mRNA translation of aminoacid regulator gene cpcA of filamentous fungus Aspergillus nidulans
Autore:
Hoffmann, B; Valerius, O; Andermann, M; Braus, GH;
Indirizzi:
Univ Gottingen, Inst Microbiol & Genet, D-37077 Gottingen, Germany Univ Gottingen Gottingen Germany D-37077 net, D-37077 Gottingen, Germany
Titolo Testata:
MOLECULAR BIOLOGY OF THE CELL
fascicolo: 9, volume: 12, anno: 2001,
pagine: 2846 - 2857
SICI:
1059-1524(200109)12:9<2846:TAAIOM>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
CROSS-PATHWAY REGULATION; DNA-BINDING PROTEIN; NEUROSPORA-CRASSA; GCN4 PROTEIN; C-JUN; SACCHAROMYCES-CEREVISIAE; SEXUAL DEVELOPMENT; ENCODED PROTEIN; LEUCINE-ZIPPER; YEAST GCN4;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Braus, GH Univ Gottingen, Inst Microbiol & Genet, D-37077 Gottingen, Germany Univ Gottingen Gottingen Germany D-37077 77 Gottingen, Germany
Citazione:
B. Hoffmann et al., "Transcriptional autoregulation and inhibition of mRNA translation of aminoacid regulator gene cpcA of filamentous fungus Aspergillus nidulans", MOL BIOL CE, 12(9), 2001, pp. 2846-2857

Abstract

The CPCA protein of the filamentous fungus Aspergillus nidulans is a member of the c-jun-like transcriptional activator family. It acts as central transcription factor of the cross-pathway regulatory network of amino acid biosynthesis and is functionally exchangeable for the general control transcriptional activator Gcn4p of Saccharomyces cerevisiae. In contrast to GCN4, expression of cpcA is strongly regulated by two equally important mechanisms with additive effects that lead to a fivefold increased CPCA protein amount under amino acid starvation conditions. One component of cpcA regulationinvolves a transcriptional autoregulatory mechanism via a CPCA recognitionelement (CPRE) in the cpcA promoter that causes a sevenfold increased cpcAmRNA level when cells are starved for amino acids. Point mutations in the CPRE cause a constitutively low mRNA level of cpcA and a halved protein level when amino acids are limited. Moreover, two upstream open reading frames(uORFs) in the 5 ' region of the cpcA mRNA are important for a translational regulatory mechanism. Destruction of both short uORFs results in a sixfold increased CPCA protein level under nonstarvation conditions and a 10-fold increase under starvation conditions. Mutations in both the CPRE and uORFregulatory elements lead to an intermediate effect, with a low cpcA mRNA level but a threefold increased CPCA protein level independent of amino acidavailability. These data argue for a combined regulation of cpcA that includes a translational regulation like that of yeast GCN4 as well as a transcriptional regulation like that of the mammalian jun and fos genes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 03:01:59