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We demonstrated that the transcription factor <jats:italic>Sox11<\/jats:italic> was highly expressed in the developing sensory neurons. To test the function of <jats:italic>Sox11<\/jats:italic>, we used a knockin mouse model where the entire coding region of <jats:italic>Sox11<\/jats:italic> was replaced by a LacZ reporter. The ablation of <jats:italic>Sox11<\/jats:italic> caused severe reduction in sensory neuron survival in the trigeminal and dorsal root ganglia, although it did not affect migration of neural crest cells or acquisition of major sensory neuron subtypes. We further demonstrated that ablating <jats:italic>Sox11<\/jats:italic> caused an arrest of axonal outgrowth in vivo and in vitro. This defect could not be fully rescued by blocking cell death. Our data suggest that <jats:italic>Sox11<\/jats:italic> is a key regulator of sensory neuron development. 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