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The Journal of Neuroscience, October 8, 2008, 28(41):10200-10205; doi:10.1523/JNEUROSCI.2786-08.2008

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Neurobiology of Disease
The Drosophila FMRP and LARK RNA-Binding Proteins Function Together to Regulate Eye Development and Circadian Behavior

Oyinkan Sofola,¹ Vasudha Sundram,² Fanny Ng,² Yelena Kleyner,² Joannella Morales,¹ Juan Botas,¹ F. Rob Jackson,² and David L. Nelson¹

¹Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, and ²Department of Neuroscience and Tufts Center for Neuroscience Research, Tufts University School of Medicine, Boston, Massachusetts 02111

Correspondence should be addressed to either of the following: David L. Nelson, Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, Email: nelson{at}bcm.tmc.edu; or F. Rob Jackson, Department of Neuroscience and Tufts Center for Neuroscience Research, Tufts University School of Medicine, Boston, MA 02111, Email: rob.jackson{at}tufts.edu

Fragile X syndrome (FXS) is the most common form of hereditary mental retardation. FXS patients have a deficit for the fragile X mental retardation protein (FMRP) that results in abnormal neuronal dendritic spine morphology and behavioral phenotypes, including sleep abnormalities. In a Drosophila model of FXS, flies lacking the dfmr1 protein (dFMRP) have abnormal circadian rhythms apparently as a result of altered clock output. In this study, we present biochemical and genetic evidence that dFMRP interacts with a known clock output component, the LARK RNA-binding protein. Our studies demonstrate physical interactions between dFMRP and LARK, that the two proteins are present in a complex in vivo, and that LARK promotes the stability of dFMRP. Furthermore, we show genetic interactions between the corresponding genes indicating that dFMRP and LARK function together to regulate eye development and circadian behavior.

Key words: Drosophila; circadian rhythm; RNA; protein; eye; genetics

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Received June 18, 2008; revised July 31, 2008; accepted Aug. 25, 2008.

Correspondence should be addressed to either of the following: David L. Nelson, Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, Email: nelson{at}bcm.tmc.edu; or F. Rob Jackson, Department of Neuroscience and Tufts Center for Neuroscience Research, Tufts University School of Medicine, Boston, MA 02111, Email: rob.jackson{at}tufts.edu

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