Expression of regulatory Helix-loop-helix factor Id2 protein in the developing and adult mouse retina

2004 ◽  
Author(s):  
Sze-chun Yeung
Keyword(s):  
Adult Mouse ◽  
Mouse Retina ◽  
Helix Loop Helix

scholarly journals The Basic Helix-Loop-Helix Genehesr2Promotes Gliogenesis in Mouse Retina

2001 ◽  
Vol 21 (4) ◽  
pp. 1265-1273 ◽  
Author(s):  
Tetsu Satow ◽  
Soo-Kyung Bae ◽  
Tomoyuki Inoue ◽  
Chihiro Inoue ◽  
Goichi Miyoshi ◽  
...  
Keyword(s):  
Mouse Retina ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix

scholarly journals Aint/Tacc3 Is Highly Expressed in Proliferating Mouse Tissues During Development, Spermatogenesis, and Oogenesis

2003 ◽  
Vol 51 (4) ◽  
pp. 455-469 ◽  
Author(s):  
Marjo Aitola ◽  
Christine M. Sadek ◽  
Jan-Åke Gustafsson ◽  
Markku Pelto-Huikko
Keyword(s):  
Adult Mouse ◽  
Coiled Coil ◽  
Proliferating Cells ◽  
Helix Loop Helix ◽  
Aryl Hydrocarbon ◽  
Spatiotemporal Expression ◽  
Mouse Tissues ◽  
Murine Homologue

Aint was originally identified on the basis of its interaction in vitro with the aryl hydrocarbon nuclear receptor translocator (Arnt). Arnt is a common heterodimerization partner in the basic helix-loop–helix (bHLH)-PER-ARNT-SIM (PAS) protein family and is involved in diverse biological functions. These include xenobiotic metabolism, hypoxic response, and circadian rhythm. In addition, Arnt has a crucial role during development. Aint is a member of a growing family of transforming acidic coiled-coil (TACC) proteins and is the murine homologue of human TACC3. Here we report the spatiotemporal expression of Tacc3 mRNA and protein in embryonic, postnatally developing, and adult mouse tissues using in situ hybridization and immunocytochemistry. Tacc3 mRNA was highly expressed in proliferating cells of several organs during murine development. However, the only adult tissues expressing high levels were testis and ovary. Immunocytochemistry revealed that Tacc3 is a nuclear protein. Our results suggest that Tacc3 has an important role in murine development, spermatogenesis, and oogenesis.

scholarly journals STAT pathway activation limits the Ascl1-mediated chromatin remodeling required for neural regeneration from Müller glia in adult mouse retina

2019 ◽  
Author(s):  
Nikolas L. Jorstad ◽  
Matthew S. Wilken ◽  
Levi Todd ◽  
Paul Nakamura ◽  
Nick Radulovich ◽  
...  
Keyword(s):  
Adult Mouse ◽  
Neural Regeneration ◽  
Mouse Retina ◽  
Binding Motif ◽  
Muller Glia ◽  
Müller Glia ◽  
Rna Seq ◽  
Transgenic Expression ◽  
Pathway Activation ◽  
Stat Pathway

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.

scholarly journals The initiation of Otx2 expression in the developing mouse retina requires a unique enhancer and either Ascl1 or Neurog2 activity

Development ◽  
2021 ◽  
Author(s):  
Michael L. Kaufman ◽  
Noah B. Goodson ◽  
Ko Uoon Park ◽  
Michael Schwanke ◽  
Emma Office ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Binding Sites ◽  
Cell Formation ◽  
Mouse Retina ◽  
Bhlh Transcription Factor ◽  
Enhancer Element ◽  
Retinal Progenitor ◽  
Helix Loop Helix ◽  
Bhlh Factors ◽  
Simultaneous Loss

During retinal development, a large subset of progenitors upregulates the transcription factor Otx2, which is required for photoreceptor and bipolar cell formation. How these retinal progenitor cells initially activate Otx2 expression is unclear. To address this, we investigated the cis-regulatory network that controls Otx2 expression. We identified a minimal enhancer element, DHS-4D, that drove expression in newly formed OTX2+ cells. CRISPR/Cas9 mediated deletion of DHS-4D reduced OTX2 expression, but this effect was diminished in postnatal development. Systematic mutagenesis of the enhancer revealed that three basic helix-loop-helix (bHLH) transcription factor binding sites were required for its activity. Single cell RNA-sequencing of nascent Otx2+ cells identified the bHLH factors Ascl1 and Neurog2 as candidate regulators. CRISPR/Cas9 targeting of these factors showed that only the simultaneous loss of Ascl1 and Neurog2 prevented OTX2 expression. Our findings suggest that Ascl1 and Neurog2 act redundantly or in a compensatory fashion to activate the DHS-4D enhancer and Otx2 expression. We observed redundancy or compensation at both the transcriptional and enhancer utilization levels, suggesting that the mechanisms governing Otx2 regulation in the retina are flexible and robust.

scholarly journals Expression of the putative microRNA processing protein, Ars2, in the developing and adult mouse retina

2009 ◽  
Vol 331 (2) ◽  
pp. 511 ◽  
Author(s):  
Robert L. Chow ◽  
Phil E. Nickerson ◽  
Perry L. Howard
Keyword(s):  
Adult Mouse ◽  
Mouse Retina ◽  
Microrna Processing

scholarly journals Otx2 Gene Deletion in Adult Mouse Retina Induces Rapid RPE Dystrophy and Slow Photoreceptor Degeneration

PLoS ONE ◽  
2010 ◽  
Vol 5 (7) ◽  
pp. e11673 ◽  
Author(s):  
Francis Béby ◽  
Michael Housset ◽  
Nicolas Fossat ◽  
Coralie Le Greneur ◽  
Frédéric Flamant ◽  
...  
Keyword(s):  
Gene Deletion ◽  
Adult Mouse ◽  
Mouse Retina ◽  
Photoreceptor Degeneration

Coexistence of neurofilaments and vimentin in a neurone of adult mouse retina

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

Increased Integration of Transplanted CD73-Positive Photoreceptor Precursors into Adult Mouse Retina

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