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The Homologous Drosophila Transcriptional Adaptors ADA2a and ADA2b Are both Required for Normal Development but Have Different Functions

Tibor Pankotai,¹ Orbán Komonyi,¹ László Bodai,¹ Zsuzsanna Újfaludi,¹ Selen Muratoglu,^2, Anita Ciurciu,¹ László Tora,³ János Szabad,⁴ and Imre Boros^1,2*

Department of Genetics and Molecular Biology, University of Szeged, Közép Fasor 52, H-6726 Szeged, Hungary,¹ Institute of Biochemistry, Biological Research Center, Temesvári Krt. 62, H-6726 Szeged, Hungary,² Institut de Génétique et de Biologie Moléculaire et Cellulaire, UMR 7104, BP 10142, 67404 Illkirch, Cu de Strasbourg, France,³ Department of Biology, Faculty of Medicine, University of Szeged, and Maternal Effect and Embryogenesis Group of the Hungarian Academy of Sciences, Somogyi B. U. 4, H-6720 Szeged, Hungary⁴

Received 7 February 2005/ Returned for modification 6 April 2005/ Accepted 6 June 2005

In Drosophila and several other metazoan organisms, there are two genes that encode related but distinct homologs of ADA2-type transcriptional adaptors. Here we describe mutations of the two Ada2 genes of Drosophila melanogaster. By using mutant Drosophila lines, which allow the functional study of individual ADA2s, we demonstrate that both Drosophila Ada2 genes are essential. Ada2a and Ada2b null homozygotes are late-larva and late-pupa lethal, respectively. Double mutants have a phenotype identical to that of the Ada2a mutant. The overproduction of ADA2a protein from transgenes cannot rescue the defects resulting from the loss of Ada2b, nor does complementation work vice versa, indicating that the two Ada2 genes of Drosophila have different functions. An analysis of germ line mosaics generated by pole-cell transplantation revealed that the Ada2a function (similar to that reported for Ada2b) is required in the female germ line. A loss of the function of either of the Ada2 genes interferes with cell proliferation. Interestingly, the Ada2b null mutation reduces histone H3 K14 and H3 K9 acetylation and changes TAF10 localization, while the Ada2a null mutation does not. Moreover, the two ADA2s are differently required for the expression of the rosy gene, involved in eye pigment production, and for Dmp53-mediated apoptosis. The data presented here demonstrate that the two genes encoding homologous transcriptional adaptor ADA2 proteins in Drosophila are both essential but are functionally distinct.

Present address: Pathology Department, University of Maryland, Holland Laboratory, 15601 Crabbs Branch Way, Rockville, MD 20855.

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