4.4 Article

En1 directs superior olivary complex neuron positioning, survival, and expression of FoxP1

期刊

DEVELOPMENTAL BIOLOGY
卷 408, 期 1, 页码 99-108

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2015.10.008

关键词

Hearing; Brainstem; Auditory; Deafness; Nucleogenesis

资金

  1. Richard King Mellon Institute for Pediatric Research at the University of Pittsburgh
  2. Child Neurology Society
  3. American Hearing Research Foundation
  4. National Institute on Deafness and other Communication Disorders (NIDCD) of the National Institutes of Health (NIH) [T32DC011499]
  5. NIDCD [F32DC014896, F32DC011982]

向作者/读者索取更多资源

Little is known about the genetic pathways and transcription factors that control development and maturation of central auditory neurons. En1, a gene expressed by a subset of developing and mature superior olivary complex (SOC) cells, encodes a homeodomain transcription factor important for neuronal development in the midbrain, cerebellum, hindbrain and spinal cord. Using genetic fate-mapping techniques, we show that all En1-lineal cells in the SOC are neurons and that these neurons are glycinergic, cholinergic and GABAergic in neurotransmitter phenotype. En1 deletion does not interfere with specification or neural fate of these cells, but does cause aberrant positioning and subsequent death of all En1-lineal SOC neurons by early postnatal ages. En1-null cells also fail to express the transcription factor FoxP1, suggesting that FoxP1 lies downstream of En1. Our data define important roles for En1 in the development and maturation of a diverse group of brainstem auditory neurons. (C) 2015 Elsevier Inc. All rights reserved.

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