ADA1, A NOVEL COMPONENT OF THE ADA GCN5 COMPLEX, HAS BROADER EFFECTS THAN GCN5, ADA2, OR ADA3/

The ADA genes encode factors which are proposed to function as transcr iptional coactivators. Here we describe the cloning, sequencing, and i nitial characterization of a novel ADA gene, ADA1. Similar to the prev iously isolated ada mutants, ada1 mutants display decreases in transcr iption from various reporters. Furthermore, ADA1 interacts with the ot her ADAs in the ADA/GCN5 complex as demonstrated by partial purificati on of the complex and immunoprecipitation experiments. We estimate tha t the complex has a molecular mass of approximately 2 MDa. Previously, it had been demonstrated that ada5 mutants displayed more severe phen otypic defects than the other ada mutants (G. A. Marcus, J. Horiuchi, N. Silverman, and L. Guarente, Mel. Cell. Biol. 16:3197-3205, 1996; S. M. Roberts and F. Winston, Mel. Cell. Biol. 16:3206-3213, 1996). ada1 mutants display defects similar to those of ada5 mutants and differen t from those of the other mutants with respect to promoters affected, inositol auxotrophy, and Spt(-) phenotypes. Thus, the ADAs can be sepa rated into two classes, suggesting that the ADA/GCN5 complex may have two separate functions. We present a speculative model on the possible roles of the ADA/GCN5 complex.