The guidance of optic axons in the developing and adult mouse retina

1979 ◽  
Vol 193 (4) ◽  
pp. 763-773 ◽  
Author(s):  
Stephen Goldberg ◽  
Beryn Frank
Keyword(s):  
Development ◽  
1991 ◽  
Vol 112 (3) ◽  
pp. 693-702 ◽  
Author(s):  
P. McCaffery ◽  
P. Tempst ◽  
G. Lara ◽  
U.C. Drager

An asymmetrically distributed protein in the embryonic mouse retina was identified as an aldehyde dehydrogenase through protein microsequencing. It was characterized as a cytosolic isoform with basic isoelectric point and preference for aliphatic substrates, features that resemble those of the isoform AHD-2 which is known to oxidize retinaldehyde to retinoic acid. Immunohistochemistry with aldehyde dehydrogenase antisera showed strong labeling of the dorsal retina from the early eye vesicle stage into adulthood. In addition, optic axons originating from the dorsal retina were transiently labeled during their outgrowth phase. Whereas in the embryo the enzyme was expressed in undifferentiated cells and in neurons, in the retina of the adult mouse the asymmetrically distributed isoform was mainly expressed in Muller glia, with the number of labeled glial cells varying with retinal position.


2019 ◽  
Author(s):  
Nikolas L. Jorstad ◽  
Matthew S. Wilken ◽  
Levi Todd ◽  
Paul Nakamura ◽  
Nick Radulovich ◽  
...  

AbstractMüller glia can serve as a source for retinal regeneration in some non-mammalian vertebrates. Recently we found that this process can be induced in mouse Müller glia after injury, by combining transgenic expression of the proneural transcription factor Ascl1 and the HDAC inhibitor TSA. However, new neurons are only generated from a subset of Müller glia in this model, and identifying factors that limit Ascl1-mediated MG reprogramming could potentially make this process more efficient, and potentially useful clinically. One factor that limits neurogenesis in some non-mammalian vertebrates is the STAT pathway activation that occurs in Müller glia in response to injury. In this report, we tested whether injury induced STAT activation hampers the ability of Ascl1 to reprogram Müller glia into retinal neurons. Using a STAT inhibitor, in combination with our previously described reprogramming paradigm, we found a large increase in the ability of Müller glia to generate neurons, similar to those we described previously. Single-cell RNA-seq showed that the progenitor-like cells derived from Ascl1-expressing Müller glia have a higher level of STAT signaling than those that become neurons. Using Ascl1 ChIP-seq and DNase-seq, we found that developmentally inappropriate Ascl1 binding sites (that were unique to the overexpression context) had enrichment for the STAT binding motif. This study provides evidence that STAT pathway activation reduces the efficiency of Ascl1-mediated reprogramming in Müller glia, potentially by directing Ascl1 to inappropriate targets.


2009 ◽  
Vol 331 (2) ◽  
pp. 511 ◽  
Author(s):  
Robert L. Chow ◽  
Phil E. Nickerson ◽  
Perry L. Howard

PLoS ONE ◽  
2010 ◽  
Vol 5 (7) ◽  
pp. e11673 ◽  
Author(s):  
Francis Béby ◽  
Michael Housset ◽  
Nicolas Fossat ◽  
Coralie Le Greneur ◽  
Frédéric Flamant ◽  
...  

Nature ◽  
1983 ◽  
Vol 303 (5913) ◽  
pp. 169-172 ◽  
Author(s):  
Ursula C. Dräger
Keyword(s):  

2011 ◽  
Vol 52 (9) ◽  
pp. 6462 ◽  
Author(s):  
Dominic Eberle ◽  
Sandra Schubert ◽  
Kai Postel ◽  
Denis Corbeil ◽  
Marius Ader
Keyword(s):  

2014 ◽  
Vol 121 ◽  
pp. 42-57 ◽  
Author(s):  
Rosa M. Ferrer-Martín ◽  
David Martín-Oliva ◽  
Ana Sierra ◽  
Maria-Carmen Carrasco ◽  
María Martín-Estebané ◽  
...  

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