A role for the Drosophila fragile X-related gene in circadian output

Shunsuke B. Inoue, Masami Shimoda, Izumi Nishinokubi, Mikiko C. Siomi, Miwako Okamura, Akira Nakamura, Satoru Kobayashi, Norio Ishida, Haruhiko Siomi

Research output: Contribution to journalArticlepeer-review

98 Citations (Scopus)


Mutations that abolish expression of an X-linked gene, FMR1, result in the pathogenesis of fragile X syndrome, the most common form of inherited mental retardation [1, 2]. To understand the normal function of the FMR1 protein, we have produced fly strains bearing deletions in a Drosophila homolog of FMR1 (dfmr1). Since fragile X patients show a number of abnormal behaviors including sleep problems [3, 4], we investigated whether a loss-of-function mutation of dfmr1 affect circadian behavior [5-8]. Here we show that under constant darkness (DD), a lack of dfmr1 expression causes arrhythmic locomotor activity, but in light:dark cycles, their behavioral rhythms appear normal. In addition, the clock-controlled eclosion rhythm is normal in DFMR1-deficient flies. These results suggest that DFMR1 plays a critical role in the circadian output pathway regulating locomotor activity in Drosophila.

Original languageEnglish
Pages (from-to)1331-1335
Number of pages5
JournalCurrent Biology
Issue number15
Publication statusPublished - 2002 Aug 6
Externally publishedYes

ASJC Scopus subject areas

  • General Biochemistry,Genetics and Molecular Biology
  • General Agricultural and Biological Sciences


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