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Molecular and Cellular Biology, September 2004, p. 8080-8089, Vol. 24, No. 18
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.18.8080-8089.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Drosophila Ada2b Is Required for Viability and Normal Histone H3 Acetylation

Dai Qi,1 Jan Larsson,2 and Mattias Mannervik1*

Department of Developmental Biology, Wenner-Gren Institute, Arrheniuslaboratories E3, Stockholm University, Stockholm,1 UCMP, Umeå University, Umeå, Sweden2

Received 12 January 2004/ Returned for modification 9 March 2004/ Accepted 27 May 2004

Regulation of chromatin through histone acetylation is an important step in gene expression. The Gcn5 histone acetyltransferase is part of protein complexes, e.g., the SAGA complex, that interact with transcriptional activators, targeting the enzyme to specific promoters and assisting in recruitment of the basal RNA polymerase transcription machinery. The Ada2 protein directly binds to Gcn5 and stimulates its catalytic activity. Drosophila contains two Ada2 proteins, Drosophila Ada2a (dAda2a) and dAda2b. We have generated flies that lack dAda2b, which is part of a Drosophila SAGA-like complex. dAda2b is required for viability in Drosophila, and its deletion causes a reduction in histone H3 acetylation. A global hypoacetylation of chromatin was detected on polytene chromosomes in dAda2b mutants. This indicates that the dGcn5-dAda2b complex could have functions in addition to assisting in transcriptional activation through gene-specific acetylation. Although the Drosophila p53 protein was previously shown to interact with the SAGA-like complex in vitro, we find that p53 induction of reaper gene expression occurs normally in dAda2b mutants. Moreover, dAda2b mutant animals show excessive p53-dependent apoptosis in response to gamma radiation. Based on this result, we speculate that dAda2b may be necessary for efficient DNA repair or generation of a DNA damage signal. This could be an evolutionarily conserved function, since a yeast ada2 mutant is also sensitive to a genotoxic agent.

* Corresponding author. Mailing address: Department of Developmental Biology, Wenner-Gren Institute, Arrheniuslaboratories E3, Stockholm University, S-106 91 Stockholm, Sweden. Phone: 46-8-161565. Fax: 46-8-6126127. E-mail: mannervik{at}devbio.su.se.

Molecular and Cellular Biology, September 2004, p. 8080-8089, Vol. 24, No. 18
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.18.8080-8089.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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