Pou4f2-GFPknock-in mouse line: A model for studying retinal ganglion cell development

genesis ◽  
2016 ◽  
Vol 54 (10) ◽  
pp. 534-541 ◽  
Author(s):  
Dongwang Zheng ◽  
Xiaoyan Yang ◽  
Donglai Sheng ◽  
Dongliang Yu ◽  
Guoqing Liang ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Development ◽  
Retinal Ganglion ◽  
Mouse Line

All Brn3 genes can promote retinal ganglion cell differentiation in the chick

Development ◽  
2000 ◽  
Vol 127 (15) ◽  
pp. 3237-3247 ◽  
Author(s):  
W. Liu ◽  
S.L. Khare ◽  
X. Liang ◽  
M.A. Peters ◽  
X. Liu ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Ganglion Cells ◽  
Cell Development ◽  
Large Set ◽  
Retinal Ganglion ◽  
Pou Domain ◽  
Temporal Expression Pattern ◽  
Cell Genesis

Targeted gene disruption studies in the mouse have demonstrated crucial roles for the Brn3 POU domain transcription factor genes, Brn3a, Brn3b, Brn3c (now called Pou4f1, Pou4f2, Pou4f3, respectively) in sensorineural development and survival. During mouse retinogenesis, the Brn3b gene is expressed in a large set of postmitotic ganglion cell precursors and is required for their early and terminal differentiation. In contrast, the Brn3a and Brn3c genes, which are expressed later in ganglion cells, appear to be dispensable for ganglion cell development. To understand the mechanism that causes the functional differences of Brn3 genes in retinal development, we employed a gain-of-function approach in the chick embryo. We find that Brn3b(l) and Brn3b(s), the two isoforms encoded by the Brn3b gene, as well as Brn3a and Brn3c all have similar DNA-binding and transactivating activities. We further find that the POU domain is minimally required for these activities. Consequently, we show that all these Brn3 proteins have a similar ability to promote development of ganglion cells when ectopically expressed in retinal progenitors. During chick retinogenesis, cBrn3c instead of cBrn3b exhibits a spatial and temporal expression pattern characteristic of ganglion cell genesis and its misexpression can also increase ganglion cell production. Based on these data, we propose that all Brn3 factors are capable of promoting retinal ganglion cell development, and that this potential may be limited by the order of expression in vivo.

scholarly journals Molecular characterization and mapping of ATOH7, a human atonal homolog with a predicted role in retinal ganglion cell development

2002 ◽  
Vol 13 (2) ◽  
pp. 95-101 ◽  
Author(s):  
Nadean L. Brown ◽  
Susan L. Dagenais ◽  
Chuan-Min Chen ◽  
Tom Glaser
Keyword(s):  
Ganglion Cell ◽  
Molecular Characterization ◽  
Retinal Ganglion Cell ◽  
Cell Development ◽  
Retinal Ganglion

scholarly journals Two new genetically modified mouse alleles labeling distinct phases of retinal ganglion cell development by fluorescent proteins

2020 ◽  
Vol 249 (12) ◽  
pp. 1514-1528 ◽  
Author(s):  
Yichen Ge ◽  
Fuguo Wu ◽  
Mobin Cheng ◽  
Jonathan Bard ◽  
Xiuqian Mu
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Fluorescent Proteins ◽  
Genetically Modified ◽  
Cell Development ◽  
Retinal Ganglion

scholarly journals Disease Gene Candidates Revealed by Expression Profiling of Retinal Ganglion Cell Development

2007 ◽  
Vol 27 (32) ◽  
pp. 8593-8603 ◽  
Author(s):  
J. T. Wang ◽  
N. J. Kunzevitzky ◽  
J. C. Dugas ◽  
M. Cameron ◽  
B. A. Barres ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Expression Profiling ◽  
Disease Gene ◽  
Cell Development ◽  
Retinal Ganglion

scholarly journals Progressive optic atrophy in a retinal ganglion cell-specific mouse model of complex I deficiency

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Luyu Wang ◽  
Mikael Klingeborn ◽  
Amanda M. Travis ◽  
Ying Hao ◽  
Vadim Y. Arshavsky ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Optic Atrophy ◽  
Complex I ◽  
Time Course ◽  
Retinal Cell ◽  
Preclinical Model ◽  
Retinal Ganglion ◽  
Mouse Line

Abstract Optic atrophy resulting from retinal ganglion cell (RGC) degeneration is a prominent ocular manifestation of mitochondrial dysfunction. Although transgenic mice lacking the mitochondrial complex I accessory subunit NDUFS4 develop early-onset optic atrophy, severe systemic mitochondrial dysfunction leads to very early death and makes this mouse line impractical for studying the pathobiology of mitochondrial optic neuropathies. Theoretically, RGC-specific inactivation of ndufs4 would allow characterization of RGC degeneration over a longer time course, provided that RGC death from mitochondrial dysfunction is a cell-autonomous process. We demonstrate that the vesicular glutamate transporter VGLUT2 may be exploited to drive robust Cre recombinase expression in RGCs without any expression observed in directly neighboring retinal cell types. Deletion of ndufs4 in RGCs resulted in reduced expression of NDUFS4 protein within the optic nerves of Vglut2-Cre;ndufs4loxP/loxP mice. RGC degeneration in Vglut2-Cre;ndufs4loxP/loxP retinas commenced around postnatal day 45 (P45) and progressed to loss of two-thirds of RGCs by P90, confirming that intrinsic complex I dysfunction is sufficient to induce RGC death. The rapidly-developing optic atrophy makes the Vglut2-Cre;ndufs4loxP/loxP mouse line a promising preclinical model for testing therapies for currently untreatable mitochondrial optic neuropathies such as Leber Hereditary Optic Neuropathy.

Extrinsic determinants of retinal ganglion cell development in primates

1989 ◽  
Vol 286 (2) ◽  
pp. 170-189 ◽  
Author(s):  
Audie G. Leventhal ◽  
Steven J. Ault ◽  
Damgmar J. Vitek ◽  
Tiande Shou
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Development ◽  
Retinal Ganglion

Human retinal ganglion cell development in early prenatal period using carbocyanine dye DiI

1993 ◽  
Vol 157 (2) ◽  
pp. 175-178 ◽  
Author(s):  
Shashi Wadhwa ◽  
Geeta Jotwani ◽  
Veena Bijlani
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Development ◽  
Prenatal Period ◽  
Retinal Ganglion ◽  
Carbocyanine Dye
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