GCN5 (General Control Non-repressed protein 5) plays a central role in the regulation of gene expression through its histone acetyltransferase (HAT) activity. Within the SAGA complex (Spt-Ada-Gcn5 acetyltransferase), GCN5 regulates transcription by modifying the chromatin structure and thus influencing the accessibility of gene promoters. Its conservation in all eukaryotes underscores its essential role in cell biology. Remarkably, among invertebrates, Toxoplasma possesses two HAT variants of the GCN5 family. GCN5a plays an important role in parasite gene expression under alkaline conditions, but is not critical for growth. In contrast, GCN5b is essential for parasite survival. Previous pioneering studies have begun to elucidate the unique molecular properties of GCN5b HAT activity, but also its partnership. However, these studies were performed on zoites still expressing the native GCN5b gene, which may lead to potentially misleading or incomplete conclusions. Here, we re-examine the unique interactome associated with the native GCN5b protein and we investigate the transcriptional consequences of depleting the protein using auxin-inducible degron technology. We are also investigating the interplay between GCN5b and its counterpart HDAC3 at the chromatin level as the parasite transitions from the tachyzoite to the merozoite stage. We will analyze their selective engagement as activator, repressor or chromatin insulator using ChIP-seq and try to decipher the "histone code" that ensures precise spatial and temporal regulation of stage-specific genes. We are also comparing the dynamics of the Toxoplasma SAGA complex between the two different zoite populations, focusing on the DNA-targeting AP2 transcription factors, but also on the PHD-containing histone PTM reader identified in the interactome of GCN5b.