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Nucleic Acids Research Advance Access published online on September 8, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp722
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© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

The loss of histone H3 lysine 9 acetylation due to dSAGA-specific dAda2b mutation influences the expression of only a small subset of genes

Nóra Zsindely1, Tibor Pankotai1, Zsuzsanna Újfaludi1, Dániel Lakatos1, Orbán Komonyi1, László Bodai1, László Tora2 and Imre M. Boros1,3,*

1Chromatin Research Group of HAS, Department of Biochemistry and Molecular Biology, University of Szeged, Közép fasor 52, H-6726 Szeged, Hungary, 2Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), UMR 7104, CNRS, ULP, INSERM U 596, Parc d’Innovation, 1, rue’ Laurent Fries, BP 10142–67404 ILLKIRCH Cedex, CU de Strasbourg, France and 3Institute of Biochemistry, Biological Research Center, Temesvári krt. 62, H-6726 Szeged, Hungary

*To whom correspondence should be addressed. Tel: +36 62 544686; Fax: +36 62 544651; Email: borosi{at}bio.u-szeged.hu

Received March 22, 2009. Revised July 23, 2009. Accepted August 16, 2009.

In Drosophila, the dADA2b-containing dSAGA complex is involved in histone H3 lysine 9 and 14 acetylation. Curiously, although the lysine 9- and 14-acetylated histone H3 levels are drastically reduced in dAda2b mutants, these animals survive until a late developmental stage. To study the molecular consequences of the loss of histone H3 lysine 9 and 14 acetylation, we compared the total messenger ribonucleic acid (mRNA) profiles of wild type and dAda2b mutant animals at two developmental stages. Global gene expression profiling indicates that the loss of dSAGA-specific H3 lysine 9 and 14 acetylation results in the expression change (up- or down-regulation) of a rather small subset of genes and does not cause a general transcription de-regulation. Among the genes up-regulated in dAda2b mutants, particularly high numbers are those which play roles in antimicrobial defense mechanisms. Results of chromatin immunoprecipitation experiments indicate that in dAda2b mutants, the lysine 9-acetylated histone H3 levels are decreased both at dSAGA up- and down-regulated genes. In contrast to that, in the promoters of dSAGA-independent ribosomal protein genes a high level of histone H3K9ac is maintained in dAda2b mutants. Our data suggest that by acetylating H3 at lysine 9, dSAGA modifies Pol II accessibility to specific promoters differently.

The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.


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