A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Reynolds-Kenneally, J., Mlodzik, M. (2005). Notch signaling controls proliferation through cell-autonomous and non-autonomous mechanisms in the Drosophila eye.  Dev. Biol. 285(1): 38--48. (Export to RIS)
FlyBase ID FBrf0187397
Publication Type Research paper
PubMed ID 16039641
PubMed Abstract During Drosophila eye development, localized Notch signaling at the dorsal ventral (DV)-midline promotes growth of the entire eye field. This long-range action of Notch signaling may be mediated through the diffusible ligand of the Jak/STAT pathway, Unpaired (Upd), which was recently identified as a downstream target of Notch. However, Notch activity has not been shown to be cell-autonomously required for Upd expression and therefore yet another diffusible signal may be required for Notch activation of Upd. Our results clarify the Notch requirement, demonstrating that Notch activity at the DV-midline leads to cell-autonomous expression of Upd as monitored in loss and gain-of-function Notch clones. In addition, mutations in the Jak/STAT pathway interact genetically with the Notch pathway by suppressing Notch mediated overgrowth. N(act) clones show non-autonomous effects on the cell cycle anterior to the furrow, indicating function of the Jak/STAT pathway. However, cell-autonomous effects of Notch within and posterior to the furrow are independent of Upd. Here, Notch autonomously maintains cells in a proliferative state and blocks photoreceptor differentiation.
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Language of Publication English
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Publication Type Journal
Abbreviation Dev. Biol.
Title Developmental Biology
Publication Year 1959-
ISBN/ISSN 0012-1606
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