Publication
Circadian Rhythm-Dependent Alterations of Gene Expression in Drosophila Brain Lacking Fragile X Mental Retardation Protein
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- Last modified
- 03/05/2025
- Type of Material
- Authors
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Shunliang Xu, Shandong UniversityMickael Poidevin, Emory UniversityEnji Han, Shandong UniversityJianzhong Bi, Shandong UniversityPeng Jin, Emory University
- Language
- English
- Date
- 2012-05-24
- Publisher
- Public Library of Science
- Publication Version
- Copyright Statement
- © 2012 Xu et al.
- License
- Final Published Version (URL)
- Title of Journal or Parent Work
- ISSN
- 1932-6203
- Volume
- 7
- Issue
- 5
- Start Page
- e37937
- End Page
- e37937
- Grant/Funding Information
- The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the Robert Wood Johnson Foundation.
- No additional external funding received for this study.
- This work was supported by NIH grant R01 MH076090 to P.J. S.X. is supported by Shandong Provincial Natural Science Foundation, China (ZR2011LH021) and Independent Innovation Foundation of Shandong University, IIFSDU (2010JC016).
- Abstract
- Fragile X syndrome is caused by the loss of the FMR1 gene product, fragile X mental retardation protein (FMRP). The loss of FMRP leads to altered circadian rhythm behaviors in both mouse and Drosophila; however, the molecular mechanism behind this phenomenon remains elusive. Here we performed a series of gene expression analyses, including of both mRNAs and microRNAs (miRNAs), and identified a number of mRNAs and miRNAs (miRNA-1 and miRNA-281) with circadian rhythm-dependent altered expression in dfmr1 mutant flies. Identification of these RNAs lays the foundation for future investigations of the molecular pathway(s) underlying the altered circadian rhythms associated with loss of dFmr1.
- Author Notes
- Keywords
- Research Categories
- Health Sciences, Medicine and Surgery
- Biology, Animal Physiology
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