S-Nitrosylation in neurogenesis and neuronal development

• S-Nitrosylation networks modulate neuronal differentiation and development.
• S-Nitrosylated GAPDH/Siah/CREB cascade controls dendritic growth.
• S-Nitrosylation of MAP1B regulates axonal retraction
• S-Nitrosylation of MEF2 serves as a negative switch for adult neurogenesis.

BackgroundNitric oxide (NO) is a pleiotropic messenger molecule. The multidimensional actions of NO species are, in part, mediated by their redox nature. Oxidative posttranslational modification of cysteine residues to regulate protein function, termed S-nitrosylation, constitutes a major form of redox-based signaling by NO.Scope of reviewS-Nitrosylation directly modifies a number of cytoplasmic and nuclear proteins in neurons. S-Nitrosylation modulates neuronal development by reaction with specific proteins, including the transcription factor MEF2. This review focuses on the impact of S-nitrosylation on neurogenesis and neuronal development.Major conclusionsFunctional characterization of S-nitrosylated proteins that regulate neuronal development represents a rapidly emerging field. Recent studies reveal that S-nitrosylation-mediated redox signaling plays an important role in several biological processes essential for neuronal differentiation and maturation.General significanceInvestigation of S-nitrosylation in the nervous system has elucidated new molecular and cellular mechanisms for neuronal development. S-Nitrosylated proteins in signaling networks modulate key events in brain development. Dysregulation of this redox-signaling pathway may contribute to neurodevelopmental disabilities such as autism spectrum disorder (ASD). Thus, further elucidation of the involvement of S-nitrosylation in brain development may offer potential therapeutic avenues for neurodevelopmental disorders.This article is part of a Special Issue entitled Redox regulation of differentiation and de-differentiation.