Xpd, a DNA helicase, classically known to play a role in transcription and nucleotide excision repair, has also been shown to be involved in cell cycle regulation in young Drosophila embryos (Chen et al., 2003, Li et al., 2010). Xpd has been shown to perform its functions as part of the TFIIH, the Cdk Activating Kinase (CAK) complex and the Crumbs/Galla-2 complex (Yeom et al., 2014). In our study of early Drosophila embryos, we report the interaction of Xpd with the Mms19 protein, which together form a complex consisting of Xpd/Mms19/Galla-2. Further investigations of the mms19 gene revealed that the knockdown of the maternal mms19 product in early embryos causes mitotic defects. We observed mainly chromosome segregation defects and spindle abnormalities. Interestingly, homozygous mms19 mutants fail to develop imaginal discs during the larval stages, a typical phenotype of a loss-of-function mutation in a mitotic gene. Epistasis studies conducted in these larvae led to the rescue of some of the mms19 phenotypes by the over expression of CAK. Our research indicates that the interactions of Xpd with Mms19 and/or Cdk7 at different stages of the cell cycle are crucial for the cell to undergo normal cell divisions.