Histone modifications are an important component of epigenetic control. Acetylation is generally associated with gene activation, whereas ubiquitination mediates both activation and repression. Histone modifying enzymes are often integrated into large multisubunit complexes. The modular SAGA chromatin-modifying complex interacts with transcription activators and the TATA-binding protein. It contains two enzymatic modules, with acetyltransferase (HAT) and deubiquitinase (DUB) activities. Using Drosophila, we sought to determine whether 1) SAGA is required for transcription of all genes, 2) SAGA dependent genes require both the HAT and DUB modules, and 3) individual modules can function independently of SAGA. We generated germline clone of genes encoding subunits of several modules to eliminate maternal gene product and examined the requirement for SAGA in oogenesis and early embryogenesis. Morphological analysis was used to determine the developmental stage at which mutants of different SAGA modules exhibit defects. Whole transcriptome profiling was used to determine which genes require different SAGA subunits. Lastly, ChIP-seq analysis was used to identify the direct targets of SAGA and its submodules in early embryos. We found that oogenesis is blocked upon loss of Ada2b, a subunit of the HAT module, whereas, germline clone females of Ataxin-7 and non-stop mutants, which are subunits of the DUB module, lay fertilized eggs with no overt defects until cellularization. These findings suggest that transcription essential for oogenesis requires the HAT activity but not the DUB activity of SAGA. Segmentation and D/V patterning appears to occur in embryos lacking the DUB module, as visualized by expression of eve and twi, but these embryos exhibit defects in cellularization. Consistent with this observation, some of the genes involved in cellularization are down regulated in Ataxin-7 GLCs. Whole genome profiling by RNA-seq shows that transcription of a subset of genes, primarily those involved in developmental, are affected by loss of Ataxin-7. ChIP-seq analysis of wild-type embryos revealed that SAGA (monitored by Ada2b) was bound at many, but not all sites bound by polII. Interestingly, ChIP-seq of DUB module proteins revealed their binding to SAGA-bound sites as well as novel sites. In summary, our data suggests that SAGA binds to only a subset of genes in the early embryos, and the DUB module is not required by all of these genes. Moreover, our data is the first to reveal that the DUB module can exist as a free form in wild type embryos that binds to novel locations in the genome.