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Pregled bibliografske jedinice broj: 161798

Mitochondrial dysfunction enhances Gal4 dependent transcription


Jeličić, Branka; Traven, Ana; Filić, Vedrana; Sopta, Mary
Mitochondrial dysfunction enhances Gal4 dependent transcription // FEMS microbiology letters, 253 (2005), 2; 207-213 doi:10.1016/j.femsle.2005.09.033 (međunarodna recenzija, članak, znanstveni)


Naslov
Mitochondrial dysfunction enhances Gal4 dependent transcription

Autori
Jeličić, Branka ; Traven, Ana ; Filić, Vedrana ; Sopta, Mary

Izvornik
FEMS microbiology letters (0378-1097) 253 (2005), 2; 207-213

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
Yeast ; transcription ; Gal4 ; Srb10 ; mitochondria

Sažetak
Cells commonly regulate gene expression in response to changing nutrient conditions in the environment. One of the most highly characterized such systems is that of the galactose induced regulon in the yeast Saccharomyces cerevisiae. In this report we have analyzed the influence of mitochondrial dysfunction on Gal4 activity and show that cells lacking mtDNA (petites) increase Gal4-dependent transcription. The DNA-binding and activation domains of Gal4 are sufficient for this effect. Furthermore, the cyclin dependent kinase Srb10 is necessary for the signaling from mitochondria to Gal4, but this effect is independent of Gal4 S699 phosphorylation or repression by Gal80. Mitochondrial dysfunction appears to affect Gal4 at the level of binding to DNA. We suggest that Srb10 dependent phosphorylation of a yet unidentified site, potentially in the Gal4 DNA binding domain, or modification of other transcription factors that cooperate with Gal4 in the process of transcriptional activation underlies the effect of Srb10 on Gal4 transcription in response to mitochondrial dysfunction.

Izvorni jezik
Engleski

Znanstvena područja
Biologija



POVEZANOST RADA


Projekt / tema
0098079

Ustanove
Institut "Ruđer Bošković", Zagreb

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE


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