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The Journal of Neuroscience, June 4, 2008, 28(23):6010-6021; doi:10.1523/JNEUROSCI.0101-08.2008

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Neurobiology of Disease
Axonal Injury and Regeneration in the Adult Brain of Drosophila

Derya Ayaz,^1,2,3 * Maarten Leyssen,^1,2 * Marta Koch,^1,2 Jiekun Yan,^1,2 Mohammed Srahna,^1,2 Vasu Sheeba,⁵ Keri J. Fogle,⁵ Todd C. Holmes,⁵ and Bassem A. Hassan^1,2,3,4

¹Laboratory of Neurogenetics, Department of Molecular and Developmental Genetics, Flanders Institute for Biotechnology (VIB), 3000 Leuven, Belgium, ²Department of Human Genetics, Katholieke Universiteit (K.U.) Leuven School of Medicine, 3000 Leuven, Belgium, Doctoral Programs in ³Molecular and Developmental Genetics and ⁴Molecular and Cognitive Neuroscience, K.U. Leuven Group Biomedicine, 3000 Leuven, Belgium, and ⁵Department of Physiology and Biophysics, University of California at Irvine, Irvine, California 92697

Correspondence should be addressed to Bassem A. Hassan, Laboratory of Neurogenetics, Department of Molecular and Developmental Genetics, Flanders Institute for Biotechnology (VIB), 3000 Leuven, Belgium. Email: bassem.hassan{at}med.kuleuven.be

Drosophila melanogaster is a leading genetic model system in nervous system development and disease research. Using the power of fly genetics in traumatic axonal injury research will significantly speed up the characterization of molecular processes that control axonal regeneration in the CNS. We developed a versatile and physiologically robust preparation for the long-term culture of the whole Drosophila brain. We use this method to develop a novel Drosophila model for CNS axonal injury and regeneration. We first show that, similar to mammalian CNS axons, injured adult wild-type fly CNS axons fail to regenerate, whereas adult-specific enhancement of protein kinase A activity increases the regenerative capacity of lesioned neurons. Combined, these observations suggest conservation of neuronal regeneration mechanisms after injury. We next exploit this model to explore pathways that induce robust regeneration and find that adult-specific activation of c-Jun N-terminal protein kinase signaling is sufficient for de novo CNS axonal regeneration injury, including the growth of new axons past the lesion site and into the normal target area.

Key words: axon; Drosophila; explant; injury; regeneration; signal transduction

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Received Jan. 10, 2008; revised April 18, 2008; accepted April 21, 2008.

Correspondence should be addressed to Bassem A. Hassan, Laboratory of Neurogenetics, Department of Molecular and Developmental Genetics, Flanders Institute for Biotechnology (VIB), 3000 Leuven, Belgium. Email: bassem.hassan{at}med.kuleuven.be

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