The PIWI interacting RNA pathway silences transposons and maintains genome integrity during germline development. In Drosophila, piRNA precursors are generated from discrete genomic loci, called piRNA clusters. The nuclear factors Rhino, Cutoff and Deadlock appear to be dedicated to processing germline cluster transcripts in Drosophila ovaries, and all three proteins localize to germline cluster chromatin. Germline cluster transcripts are not spliced, and mutations in rhino, cuff and deadlock that block piRNA production also lead to cluster transcript splicing. UAP56 is an ATP dependent RNA binding protein that functions in general mRNP biogenesis. We previously showed that UAP56 interacts with piRNA precursors and that a point mutation in UAP56 (uap56-sz15) predicted to weaken RNA binding specifically disrupts piRNA biogenesis and increases cluster transcript splicing. The THO complex and UAP56 forms the evolutionarily conserved TREX (transcription/export) complex. Using immunoaffinity purification and mass spectroscopy from fly ovaries lysate, we confirm the Drosophila UAP56 interacts with the THO complex. Significantly, we also show that this point mutation in uap56-sz15 significantly reduces binding to the THO complex. We also show that THO complex components co-localize to nuclear foci with Rhino. Similar to UAP56, THO complex binds specifically to unsplicing cluster transcripts. Mutation in thoc7, one of the core components of the THO complex, disrupts localization of Rhino, Cuff and UAP56. It also blocks piRNA production and leads to global defects in transposons silencing. In addition, thoc7 mutation increases cluster transcript splicing. We propose that stable cluster transcripts binding by the TREX complex is required to suppress piRNA precursor splicing, and promotes cluster chromatin assembly.