The nervous system plays an important role in modulating several physiological processes and complex behaviors in multicellular animals. Drosophila has served as an excellent model to unravel the neuronal regulation of multiple complex behaviors like memory and learning, aggression, courtship and female reproduction. The neuronal regulation of female reproduction in particular has been studied extensively and the multiple circuits which play a major role have been identified. Several studies have shown that octopaminergic neurons from the MK-0683 central nervous system regulate multiple female reproductive behaviors like ovulation, egg laying and also sperm release. An ex vivo study has demonstrated the direct role of octopamine in the contraction of the Drosophila female reproductive tract. Glutamatergic neurons also modulate the contraction of oviduct by acting in conjunction with octopamine during egg laying. A recent study has revealed that octopamine brings about the contraction/relaxation of oviduct through CamKII mediated signaling in the epithelial cells of oviduct. Apart from neuronal circuits intrinsic to the female, seminal proteins transferred from the male during copulation are also essential for inducing post mating behaviors in female through these neuronal circuits. For example, Sex peptides transferred from male into the female reproductive tract during copulation bind to receptors on the sensory neurons of the female reproductive tract, that project on to the central nervous system regions, and bring about post mating reproductive behaviors like increased ovulation, egg laying and reduced receptivity. With such well studied neuronal circuits regulating the female reproduction and simple reproductive assays, the Drosophila female reproductive system serves as a good model to understand the functions of uncharacterized genes implicated in neuronal functions. In this study, we report a novel and essential role of the Bx in Drosophila female reproduction. The Bx null females generated in this work showed normal ovariole development but with highly reduced fecundity and ovulation. Reduced fecundity correlates well with reduced ovulation. However, unlike earlier reported mutants which showed reduced fecundity and ovulation, accumulation of mature eggs in the ovaries is not seen in the Bx7 mutant females. One possible reason for this could be the highly reduced abdominal cavity caused by the distended crop. This is supported by a recent study which identified Bx in a screen for defective gastric emptying, thereby causing bulged crop. Other reason could be due to the function of Bx in the ovariole development, which was not investigated in this study. Highly reduced fertility of Bx7 mutants could be attributed to the failure of sperm release from the storage organs during ovulation. There is no direct evidence as to what stimulates the release of sperms from the storage organs in the females. One of the proposed stimuli is egg movement/presence in the uterus which activates stretch receptors in the uterus and induces release of sperm from storage organs. It is thus possible that the reduced sperm release observed in the Bx7 null females is due to reduced ovulation.