A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Williams, J.A., Su, H.S., Bernards, A., Field, J., Sehgal, A. (2001). A circadian output in Drosophila mediated by Neurofibromatosis-1 and Ras/MAPK.  Science 293(5538): 2251--2256. (Export to RIS)
FlyBase ID FBrf0138535
Publication Type Research paper
PubMed ID 11567138
PubMed Abstract Output from the circadian clock controls rhythmic behavior through poorly understood mechanisms. In Drosophila, null mutations of the neurofibromatosis-1 (Nf1) gene produce abnormalities of circadian rhythms in locomotor activity. Mutant flies show normal oscillations of the clock genes period (per) and timeless (tim) and of their corresponding proteins, but altered oscillations and levels of a clock-controlled reporter. Mitogen-activated protein kinase (MAPK) activity is increased in Nf1 mutants, and the circadian phenotype is rescued by loss-of-function mutations in the Ras/MAPK pathway. Thus, Nf1 signals through Ras/MAPK in Drosophila. Immunohistochemical staining revealed a circadian oscillation of phospho-MAPK in the vicinity of nerve terminals containing pigment-dispersing factor (PDF), a secreted output from clock cells, suggesting a coupling of PDF to Ras/MAPK signaling.
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Supplementary material A circadian output in Drosophila mediated by Neurofibromatosis-1 and Ras/MAPK. [FBrf0141792]

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Title Science
Publication Year 1895-
ISBN/ISSN 0036-8075
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