Mukhopadhyay Abhishek, Jarrett Jennifer, Chlon Timothy, Kessler John A
Department of Neurology, Northwestern University's Feinberg School of Medicine, Chicago, IL 60611, USA.
Dev Biol. 2009 Oct 1;334(1):142-51. doi: 10.1016/j.ydbio.2009.07.018. Epub 2009 Jul 22.
The basic-helix-loop-helix transcription factor HeyL is expressed at high levels by neural crest progenitor cells (NCPs) that give rise to neurons and glia in dorsal root ganglia (DRG). Since HeyL expression was observed in these NCPs during the period of neurogenesis, we generated HeyL null mutants to help examine the factor's role in ganglion neuronal specification. Homozygous null mutation of HeyL reduced the number of TrkC(+) neurons in DRG at birth including the subpopulation that expresses the ETS transcription factor ER81. Conversely, null mutation of the Hey paralog, Hey1, increased the number of TrkC(+) neurons. Null mutation of HeyL increased expression of the Hey paralogs Hey1 and Hey2, suggesting that HeyL normally inhibits their expression. Double null mutation of both Hey1 and HeyL rescued TrkC(+) neuron numbers to control levels. Thus, the balance between HeyL and Hey1 expression regulates the differentiation of a subpopulation of TrkC(+) neurons in the DRG.
碱性螺旋-环-螺旋转录因子HeyL在神经嵴祖细胞（NCPs）中高表达，这些细胞可分化为背根神经节（DRG）中的神经元和神经胶质细胞。由于在神经发生期间在这些NCPs中观察到HeyL表达，我们生成了HeyL基因敲除突变体，以帮助研究该因子在神经节神经元特化中的作用。HeyL的纯合缺失突变减少了出生时DRG中TrkC(+)神经元的数量，包括表达ETS转录因子ER81的亚群。相反，Hey的旁系同源物Hey1的缺失突变增加了TrkC(+)神经元的数量。HeyL的缺失突变增加了Hey旁系同源物Hey1和Hey2的表达，表明HeyL通常抑制它们的表达。Hey1和HeyL的双缺失突变将TrkC(+)神经元数量恢复到对照水平。因此，HeyL和Hey1表达之间的平衡调节了DRG中TrkC(+)神经元亚群的分化。
