Morphologies of mouse retinal ganglion cells expressing transcription factors Brn3a, Brn3b, and Brn3c: Analysis of wild type and mutant cells using genetically-directed sparse labeling

被引:75
作者
Badea, Tudor Constantin [1 ,4 ]
Nathans, Jeremy [1 ,2 ,3 ]
机构
[1] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Dept Mol Biol & Genet, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Dept Neurosci, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Dept Ophthalmol, Baltimore, MD 21205 USA
[4] NEI, Retinal Circuit Dev & Genet Unit, Neurobiol Neurodegenerat & Repair Lab, Bethesda, MD 20892 USA
关键词
Mouse; Retina development; Retinal ganglion cell; Brn3 transcription factors; Dendritic arbor; LATERAL GENICULATE-NUCLEUS; MAMMALIAN RETINA; PRIMATE RETINA; BIPOLAR CELLS; CATS RETINA; DENDRITIC MORPHOLOGIES; RECEPTIVE-FIELDS; AXON OUTGROWTH; VISUAL-SYSTEM; FACTOR BRN-3B;
D O I
10.1016/j.visres.2010.08.039
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The mammalian retina contains more than 50 distinct neuronal types, which are broadly classified into several major classes: photoreceptor, bipolar, horizontal, amacrine, and ganglion cells. Although some of the developmental mechanisms involved in the differentiation of retinal ganglion cells (RGCs) are beginning to be understood, there is little information regarding the genetic and molecular determinants of the distinct morphologies of the 15-20 mammalian RGC cell types. Previous work has shown that the transcription factor Brn3b/Pou4f2 plays a major role in the development and survival of many RGCs. The roles of the closely related family members, Brn3a/Pou4f1 and Brn3c/Pou4f3 in RGC development are less clear. Using a genetically-directed method for sparse cell labeling and sparse conditional gene ablation in mice, we describe here the sets of RGC types in which each of the three Brn3/Pou4f transcription factors are expressed and the consequences of ablating these factors on the development of RGC morphologies. Published by Elsevier Ltd.
引用
收藏
页码:269 / 279
页数:11
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