Naslov
Functional interplay between SWI/SNF and RSC chromatin-remodelling complexes at the yeast PHO5 promoter

Autori
Musladin, Sanja ; Korber, Philipp ; Barbarić, Slobodan

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Book of Abstracts of the 3rd SFB TR5 Symposium "Chromatin - Assembly and Inheritance of Functional States" / - München, 2010, 87-87

Skup
3rd SFB TR5 Symposium "Chromatin - Assembly and Inheritance of Functional States"

Mjesto i datum
München, Njemačka, 06.10.2010. - 08.10.2010

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
transcriptional regulation; chromatin remodelling; yeast PHO genes

Sažetak
The yeast PHO5 promoter has been a very useful model in elucidating the relationship between chromatin structure remodelling and gene regulation. The massive transition of chromatin structure at the PHO5 promoter from a repressed, closed, to an active, open state was clearly demonstrated to be a prerequisite for gene transcription. Chromatin remodelling is mediated by chromatin-modifying and -remodelling complexes and histone chaperones. We have previously shown for the PHO5 promoter that the SWI/SNF and Ino80 remodelling complexes, the Gcn5 HAT activity and the histone chaperone Asf1 were involved, but no essential chromatin cofactor has been identified yet. The RSC complex, one of the most abundant chromatin-remodelling complexes in yeast, whose ATPase subunit STH1 is a paralogue of SNF2, has recently been shown to disassemble nucleosomes in vitro. Here we show that the RSC complex has a prominent role in chromatin remodelling and consequently in activation of the PHO5 promoter in vivo. Since inactivation of STH1 is lethal, we employed a conditional, temperature sensitive sth1 mutant. Already at conditions that bring about the depletion rather than complete elimination of Sth1, remodelling at the PHO5 promoter was significantly affected. Upon more complete ablation of the RSC complex combined with artificial, semi-induction conditions, where higher stringency of cofactor requirements is generally observed, chromatin opening was strongly affected or even fully prevented. Simultaneous inactivation of SWI/SNF and RSC complexes completely prevented remodelling at the PHO5 promoter under physiological induction conditions, demonstrating a functional interplay of the two complexes in modulation of the promoter chromatin structure. We have previously shown that at the PHO84 promoter, which is coregulated with the PHO5 promoter, different remodelling pathways were involved in disassembly of the two neighbouring nucleosomes. Possible differential requirement for the RSC complex in remodelling of these two nucleosomes is being examined.

Izvorni jezik
Engleski

Znanstvena područja
Biotehnologija

POVEZANOST RADA