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

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 i...

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Bibliographic Details
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
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Summary: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.
ISSN:0925-4773
DOI:10.1016/S0925-4773(02)00289-7