Drosophila nemo is an essential gene involved in the regulation of programmed cell death

• Published in: Mechanisms of development 2002-11, Vol.119 (1), p.9
• Main Authors: Mirkovic, Ivana, Charish, Kristi, Gorski, Sharon M, McKnight, Kristen, Verheyen, Esther M
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Cell Death; Crosses, Genetic; Drosophila melanogaster; Drosophila Proteins; Epidermis - embryology; Epidermis - metabolism; Gene Expression Regulation, Developmental; Heterozygote; Immunohistochemistry; In Situ Nick-End Labeling; JNK Mitogen-Activated Protein Kinases; MAP Kinase Kinase 4; Mitogen-Activated Protein Kinase Kinases - metabolism; Mitogen-Activated Protein Kinases - genetics; Mitogen-Activated Protein Kinases - physiology; Phenotype; Photoreceptor Cells, Invertebrate - embryology; Signal Transduction; Time Factors; Transforming Growth Factor beta - metabolism; Transgenes
• ISSN: 0925-4773
• DOI: 10.1016/S0925-4773(02)00289-7

Nemo-like kinases define a novel family of serine/threonine kinases that are involved in integrating multiple signaling pathways. They are conserved regulators of Wnt/Wingless pathways, which may coordinate Wnt with TGFbeta-mediated signaling. Drosophila nemo was identified through its involvement in epithelial planar polarity, a process regulated by a non-canonical Wnt pathway. We have previously found that ectopic expression of Nemo using the Gal4-UAS system resulted in embryonic lethality associated with defects in patterning and head development. In this study we present our analyses of the phenotypes of germline clone-derived embryos. We observe lethality associated with head defects and reduction of programmed cell death and conclude that nmo is an essential gene. We also present data showing that nmo is involved in regulating apoptosis during eye development, based on both loss of function phenotypes and on genetic interactions with the pro-apoptotic gene reaper. Finally, we present genetic data from the adult wing that suggest the activity of ectopically expressed Nemo can be modulated by Jun N-terminal kinase (JNK) signaling. Such an observation supports the model that there is cross-talk between Wnt, TGFbeta and JNK signaling at multiple stages of development.