, 2009 and Qin et al., 2010). Collectively, these studies support the idea that transcription factors can independently regulate two different aspects of axon development, growth and guidance, by inducing different target genes according to the developmental requirements of the cell. Is axon growth regulated by epigenetic mechanisms? Compelling evidence on epigenetic mechanisms selectively regulating axon growth in the mammalian brain U0126 nmr is scarce. Epigenetic regulators including the histone acetyltransferase CBP and the chromatin modifier Sat2b influence cortical and motor neuron projection patterns, but this is also linked to a role in neuronal subtype specification (Alcamo et al., 2008,

Britanova et al., 2008 and Lee et al.,

2009). Loss of function of the methyl-CpG-binding transcriptional repressor MeCP2 has been associated with several abnormalities in neuronal morphogenesis including disrupted axon projections (Belichenko et al., 2009 and Degano et al., 2009). find more Axonal targeting defects observed in MeCP2 knockout mice are attributed to changes in the expression of the guidance factor Semaphorin3F, albeit in a non-cell-autonomous fashion (Degano et al., 2009). Among the genes identified in a screen for axonal sprouting after stroke is ATRX (α-thalassemia/mental retardation syndrome X-linked) (Li et al., 2010b), a chromatin remodeling enzyme linked to mental retardation that has also been implicated in dendrite development and neuronal survival (Bérubé et al., 2005 and Shioda et al., 2011). ATRX appears to be upregulated in sprouting neurons relative to nonsprouting

neurons. Knockdown of ATRX by RNAi reduces basal axon growth of cultured DRG neurons and prevents axonal sprouting after stroke in vivo (Li et al., 2010b). Interestingly, ATRX and MeCP2 can interact in vitro and in cells, and in MeCP2 knockout cells ATRX fails to localize to heterochromatin, displaying instead a diffuse expression pattern (Nan et al., 2007). Thus, some of the neuronal defects observed enough in MeCP2 mutants might be due to abnormal ATRX activity. Future studies will be needed to understand the extent of epigenetic mechanisms in axon growth. As the receptive limbs of neurotransmission in the brain, dendrites have evolved to display immense variety of shape and size. Dendrite architecture strongly influences the processing of information (Spruston, 2008), suggesting that the morphogenesis of dendrite arbors directly impacts the flow of information across the brain. Although we will focus on the role of transcription factors on dendrite morphology in mammalian systems, significant contributions in this field have also come from studies in the fly nervous system. We refer the reader to excellent reviews on this topic (Corty et al., 2009, Jan and Jan, 2003 and Jan and Jan, 2010).