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Pregled bibliografske jedinice broj: 305564

Increasing the rate of chromatin remodeling and gene activation - a novel role for the histone acetyltransferase Gcn5


Barbarić, Slobodan, Walker, Jane; Schmid, Andrea; Svejstrup, Jesper Q; Hoerz, Wolfram
Increasing the rate of chromatin remodeling and gene activation - a novel role for the histone acetyltransferase Gcn5 // EMBO Journal, 20 (2001), 17; 4944-4951 (međunarodna recenzija, članak, znanstveni)


CROSBI ID: 305564 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

Naslov
Increasing the rate of chromatin remodeling and gene activation - a novel role for the histone acetyltransferase Gcn5

Autori
Barbarić, Slobodan, Walker, Jane ; Schmid, Andrea ; Svejstrup, Jesper Q ; Hoerz, Wolfram

Izvornik
EMBO Journal (0261-4189) 20 (2001), 17; 4944-4951

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

Ključne riječi
GCN5; gene regulation; histone acetylation; PHO5

Sažetak
Histone acetyltransferases (HATs) such as Gcn5 play a role in transcriptional activation. However, the majority of constitutive genes show no requirement for GCN5, and even regulated genes, such as the yeast PHO5 gene, do not seem to be affected significantly by its absence under normal activation conditions. Here we show that even though the steady-state level of activated PHO5 transcription is not affected by deletion of GCN5, the rate of activation following phosphate starvation is significantly decreased. This delay in transcriptional activation is specifically due to slow chromatin remodeling of the PHO5 promoter, whereas the transmission of the phosphate starvation signal to the PHO5 promoter progresses at a normal rate. Chromatin remodeling is equally delayed in a galactose-inducible PHO5 promoter variant in which the Pho4 binding sites have been replaced by Gal4 binding sites. By contrast, activation of the GAL1 gene by galactose addition occurs with normal kinetics. Lack of the histone H4 N-termini leads to a similar delay in activation of the PHO5 promoter. These results indicate that one important contribution of HATs is to increase the rate of gene induction by accelerating chromatin remodeling, rather than to affect the final steady-state expression levels.

Izvorni jezik
Engleski

Znanstvena područja
Biotehnologija



POVEZANOST RADA


Projekti:
0058025

Ustanove:
Prehrambeno-biotehnološki fakultet, Zagreb

Profili:

Avatar Url Slobodan Barbarić (autor)


Citiraj ovu publikaciju:

Barbarić, Slobodan, Walker, Jane; Schmid, Andrea; Svejstrup, Jesper Q; Hoerz, Wolfram
Increasing the rate of chromatin remodeling and gene activation - a novel role for the histone acetyltransferase Gcn5 // EMBO Journal, 20 (2001), 17; 4944-4951 (međunarodna recenzija, članak, znanstveni)
Barbarić, Slobodan, Walker, Jane, Schmid, A., Svejstrup, J. & Hoerz, W. (2001) Increasing the rate of chromatin remodeling and gene activation - a novel role for the histone acetyltransferase Gcn5. EMBO Journal, 20 (17), 4944-4951.
@article{article, author = {Schmid, Andrea and Svejstrup, Jesper Q and Hoerz, Wolfram}, year = {2001}, pages = {4944-4951}, keywords = {GCN5, gene regulation, histone acetylation, PHO5}, journal = {EMBO Journal}, volume = {20}, number = {17}, issn = {0261-4189}, title = {Increasing the rate of chromatin remodeling and gene activation - a novel role for the histone acetyltransferase Gcn5}, keyword = {GCN5, gene regulation, histone acetylation, PHO5} }
@article{article, author = {Schmid, Andrea and Svejstrup, Jesper Q and Hoerz, Wolfram}, year = {2001}, pages = {4944-4951}, keywords = {GCN5, gene regulation, histone acetylation, PHO5}, journal = {EMBO Journal}, volume = {20}, number = {17}, issn = {0261-4189}, title = {Increasing the rate of chromatin remodeling and gene activation - a novel role for the histone acetyltransferase Gcn5}, keyword = {GCN5, gene regulation, histone acetylation, PHO5} }

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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