Hmx1 is required for the normal development of somatosensory neurons in the geniculate ganglion

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• 作者：Lely A. Quina^a ; Lynne Tempest^a ; Yun-Wei A. Hsu^a ; Timothy C. Cox^c ; ^d ; ^e ; ^f ; Eric E. Turner^a ; ^b ; ^c ; ^{eric.turner@seattlechildrens.org}
• 关键词：Hmx1 ; Homeodomain ; Geniculate ganglion ; Trigeminal ganglion ; Dorsal root ganglion ; Posterior auricular nerve ; Neural crest
• 刊名：Developmental Biology
• 出版年：2012
• 期刊代码：167_00121606
• 类别：bio
• 出版时间：1 May, 2012
• 卷：365
• 期：1
• 页码：152-163
• 文件大小：3464 K

摘要

Hmx1 is a variant homeodomain transcription factor expressed in the developing sensory nervous system, retina, and craniofacial mesenchyme. Recently, mutations at the Hmx1 locus have been linked to craniofacial defects in humans, rats, and mice, but its role in nervous system development is largely unknown. Here we show that Hmx1 is expressed in a subset of sensory neurons in the cranial and dorsal root ganglia which does not correspond to any specific sensory modality. Sensory neurons in the dorsal root and trigeminal ganglia of Hmx1^dm/dm mouse embryos have no detectable Hmx1 protein, yet they undergo neurogenesis and express sensory subtype markers normally, demonstrating that Hmx1 is not globally required for the specification of sensory neurons from neural crest precursors. Loss of Hmx1 expression has no obvious effect on the early development of the trigeminal (V), superior (IX/X), or dorsal root ganglia neurons in which it is expressed, but results in marked defects in the geniculate (VII) ganglion. Hmx1^dm/dm mouse embryos possess only a vestigial posterior auricular nerve, and general somatosensory neurons in the geniculate ganglion are greatly reduced by mid-gestation. Although Hmx1 is expressed in geniculate neurons prior to cell cycle exit, it does not appear to be required for neurogenesis, and the loss of geniculate neurons is likely to be the result of increased cell death. Fate mapping of neural crest-derived tissues indicates that Hmx1-expressing somatosensory neurons at different axial levels may be derived from either the neural crest or the neurogenic placodes.