TY - JOUR
T1 - En1 directs superior olivary complex neuron positioning, survival, and expression of FoxP1
AU - Altieri, Stefanie C.
AU - Jalabi, Walid
AU - Zhao, Tianna
AU - Romito-DiGiacomo, Rita R.
AU - Maricich, Stephen M.
N1 - Funding Information:
We thank members of the Maricich lab and Dr. Sharyl Fyffe-Maricich for critical discussions concerning the data and the manuscript. We thank Dr. Gary Landreth at Case Western Reserve University for supplying laboratory space to WJ. Confocal imaging was done at Children's Hospital of Pittsburgh with the generous assistance of Dr. Tim Sanders and his laboratory. This work was supported by the Richard King Mellon Institute for Pediatric Research at the University of Pittsburgh (SMM), the Child Neurology Society (SMM) , the American Hearing Research Foundation (SMM) , the National Institute on Deafness and other Communication Disorders (NIDCD) of the National Institutes of Health (NIH) T32DC011499 (SCA), NIDCD F32DC014896 (SCA) and NIDCD F32DC011982 (WJ). The authors declare no competing financial interests.
Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2015/12/1
Y1 - 2015/12/1
N2 - 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.
AB - 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.
KW - Auditory
KW - Brainstem
KW - Deafness
KW - Hearing
KW - Nucleogenesis
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U2 - 10.1016/j.ydbio.2015.10.008
DO - 10.1016/j.ydbio.2015.10.008
M3 - Article
C2 - 26542008
AN - SCOPUS:84949292808
VL - 408
SP - 99
EP - 108
JO - Developmental Biology
JF - Developmental Biology
SN - 0012-1606
IS - 1
ER -