The function of Six1 and Six4 in the development of cranial ganglia

  • Konishi Yoshiyuki
    Division of Biology Center for Molecular Medicine, Jichi Medical University

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  • 脳神経節形成におけるSix1,Six4の機能解析(平成17年度自治医科大学医学部研究奨励金研究成果報告)

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Survival of sensory neurons is tightly regulated in a cell-type and developmental-stage-specific manner. Transcriptional regulatory mechanisms underlying this regulation remain to be elucidated. In the present study, we investigated the role of Six1 and Six4 in the development of trigeminal ganglia. Abundant expression of Six1 and Six4 was noted in sensory neurons during early trigeminal gangliogenesis. Loss of both Six1 and Six4 in mice caused severe defects in the trigeminal ganglia, wherein massive apoptosis accompanied by activation of caspase-3 was observed at early but not late stages of gangliogenesis. In Six1^<-1-> Six4^<-1-> mice, trigeminal sensory neurons were generated, but showed reduced expression of Bcl-x compared to the wild-type mice. Accordingly, neurons from the deficient mice could not survive in culture even in the presence of neurotrophins. Our results suggest a cell-intrinsic role of Six1 and Six4 in the survival of early-generated trigeminal sensory neurons.

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