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The Journal of Neuroscience, June 3, 2009, 29(22):7116-7123; doi:10.1523/JNEUROSCI.5397-08.2009

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Brief Communications
Axotomy-Induced Smad1 Activation Promotes Axonal Growth in Adult Sensory Neurons

Hongyan Zou,1,2 * Carole Ho,1,3 * Karen Wong,1 and Marc Tessier-Lavigne1

1Genentech, Inc., South San Francisco, California 94080, and Departments of 2Neurosurgery and 3Neurology, Stanford University School of Medicine, Stanford, California 94305

Correspondence should be addressed to Marc Tessier-Lavigne, Genentech, Inc., South San Francisco, California 94080. Email: marctl{at}gene.com

Mature neurons have diminished intrinsic regenerative capacity. Axotomy of the peripheral branch of adult dorsal root ganglia (a "conditioning" lesion) triggers a transcription-dependent axon growth program. Here, we show that this growth program requires the function of the transcription factor Smad1. After peripheral axotomy, neuronal Smad1 is upregulated, and phosphorylated Smad1 accumulates in the nucleus. Both events precede the onset of axonal extension. Reducing Smad1 by RNA interference in vitro impairs axonal growth, and the continued presence of Smad1 is required to maintain the growth program. Furthermore, intraganglionic injection of BMP2 or 4, which activates Smad1, markedly enhances axonal growth capacity, mimicking the effect of a conditioning lesion. Thus, activation of Smad1 by axotomy is a key component of the transcriptional switch that promotes an enhanced growth state of adult sensory neurons.

Received Nov. 4, 2008; revised April 7, 2009; accepted April 8, 2009.

Correspondence should be addressed to Marc Tessier-Lavigne, Genentech, Inc., South San Francisco, California 94080. Email: marctl{at}gene.com


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[Abstract] [Full Text] [PDF]


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