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Nucleic Acids Research Advance Access published online on September 29, 2006
Nucleic Acids Research, doi:10.1093/nar/gkl678
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© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

SIR2 modifies histone H4-K16 acetylation and affects superhelicity in the ARS region of plasmid chromatin in Saccharomyces cerevisiae

Francesco Chiani, Francesca Di Felice and Giorgio Camilloni1,*

Dipartimento di Genetica e Biologia Molecolare, Università di Roma ‘La Sapienza’ Rome, Italy 1 Istituto di Biologia e Patologia Molecolari, CNR Rome, Italy

*To whom correspondence should be addressed. Tel: +390649912808; Fax: +390649912500; Email: giorgio.camilloni{at}uniroma1.it

Received March 23, 2006. Revised April 6, 2006. Accepted September 5, 2006.

The null mutation of the SIR2 gene in Saccharomyces cerevisiae has been associated with a series of different phenotypes including loss of transcriptional silencing, genome instability and replicative aging. Thus, the SIR2 gene product is an important constituent of the yeast cell. SIR2 orthologues and paralogues have been discovered in organisms ranging from bacteria to man, underscoring the pivotal role of this protein. Here we report that a plasmid introduced into sir2{Delta} cells accumulates more negative supercoils compared to the same plasmid introduced into wild-type (WT) cells. This effect appears to be directly related to SIR2 expression as shown by the reduction of negative supercoiling when SIR2 is overexpressed, and does not depend on the number or positioning of nucleosomes on plasmids. Our results indicate that this new phenotype is due to the lack of Sir2p histone deacetylase activity in the sir2{Delta} strain, because only the H4-K16 residue of the histone octamer undergoes an alteration of its acetylation state. A model proposing interference with the replication machinery is discussed.


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