Up-regulation of Cadherin-2 and Cadherin-4 in Regenerating Visual Structures of Adult Zebrafish

Liu, Q.; Londraville, Richard L.; Azodi, E.; Babb, Sherry G.; Chiappini-Williamson, C.; Marrs, James A.; Raymond, Pamela A.

doi:10.1006/exnr.2002.8008

Cited by 39 publications

(33 citation statements)

References 58 publications

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“…There is also evidence that the genetic cascades described and tested for roles during embryonic retinal neurogenesis are reengaged during the regenerative process. Early in the regeneration process, within days of the lesion, cells of the neurogenic clusters express genes typical of retinal progenitors, including pax6 (Hitchcock et al, 1996), vsx-1 (Levine et al, 1994), Notch-3 (Sullivan et al, 1997), and n-cadherin (Liu et al, 2002). Preliminary studies from our laboratory have also verified transient expression of ath5 following a ouabain lesion, similar to the transient expression of ath5 during embryonic retinal neurogenesis (Spritzer et al, 2005).…”

Section: B Stem Cells and Developmental Genetics Of Regenerationmentioning

confidence: 52%

Neurogenesis in the Fish Retina

Stenkamp

2007

International Review of Cytology

122

136

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The retinas of teleost fish have long been of interest to developmental neurobiologists for their persistent plasticity during growth, life history changes, and response to injury. Because the vertebrate retina is a highly conserved tissue, the study of persistent plasticity in teleosts has provided insights into mechanisms for postembryonic retinal neurogenesis in mammals. In addition, in the past 10 years there has been an explosion in the use of teleost fish-zebrafish (Danio rerio) in particular-to understand the mechanisms of embryonic retinal neurogenesis in a model vertebrate with genetic resources. This review summarizes the key features of teleost retinal neurogenesis that make it a productive and interesting experimental system, and focuses on the contributions to our knowledge of retinal neurogenesis that uniquely required or significantly benefited from the use of a fish model system.

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Section: B Stem Cells and Developmental Genetics Of Regenerationmentioning

confidence: 52%

Neurogenesis in the Fish Retina

Stenkamp

2007

International Review of Cytology

122

136

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“…The tightly packed clusters of progenitors surrounding each radial Müller glia is suggestive of differential cell adhesion, and we previously reported injury-induced upregulation of cdh2 transcript and N-cadherin (Cadherin 2) protein (Liu et al, 2002;Raymond et al, 2006) and N-cadherin distribution along the radial processes of Müller glia and progenitors in the neurogenic cluster (Fig.6A,B). We therefore asked whether N-cadherinmediated homophilic adhesion is responsible for the tight clustering of neuronal progenitors.…”

Section: N-cadherin Is Necessary For the Formation Of Neurogenic Clusmentioning

confidence: 58%

A self-renewing division of zebrafish Müller glial cells generates neuronal progenitors that require N-cadherin to regenerate retinal neurons

2013

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Müller glia function as retinal stem cells in adult zebrafish. In response to loss of retinal neurons, Müller glia partially dedifferentiate, re-express neuroepithelial markers and re-enter the cell cycle. We show that the immunoglobulin superfamily adhesion molecule Alcama is a novel marker of multipotent retinal stem cells, including injury-induced Müller glia, and that each Müller glial cell divides asymmetrically only once to produce an Alcama-negative, proliferating retinal progenitor. The initial mitotic division of Müller glia involves interkinetic nuclear migration, but mitosis of retinal progenitors occurs in situ. Rapidly dividing retinal progenitors form neurogenic clusters tightly associated with Alcama/N-cadherinlabeled Müller glial radial processes. Genetic suppression of Ncadherin function interferes with basal migration of retinal progenitors and subsequent regeneration of HuC/D + inner retinal neurons.

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“…A first possibility is that the WT promoter is lacking some elements repressing promoter activity in this particular glial cell type. A second more interesting possibility is that, as reported for other proteins (Ankerhold et al, 1998;Bernhardt, 1999;Liu et al, 2002;Schweitzer et al, 2003), ␣1-tubulin is upregulated in a subset of non-neuronal cells in response to optic nerve lesion.…”

Section: Discussionmentioning

confidence: 84%

An Element in the α1-Tubulin Promoter Is Necessary for Retinal Expression during Optic Nerve Regeneration But Not after Eye Injury in the Adult Zebrafish

Senut¹,

Gulati-Leekha²,

Goldman³

2004

J. Neurosci.

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We have shown previously that a 1.696 kb upstream fragment of the goldfish ␣1-tubulin promoter was capable of driving green fluorescent protein (GFP) expression in the developing and regenerating zebrafish CNS in a pattern closely mimicking the endogenous ␣1-tubulin gene. Comparison of fish and rat ␣1-tubulin promoters identified a 64 bp region with a conserved repetitive homeodomain (HD) consensus sequence core (TAAT) and a nearby basic helix-loop-helix binding E-box sequence (CANNTG), which led us to speculate that it could be of importance for regulating ␣1-tubulin gene transcription. To address this issue, we examined the ability of deletion mutants of the 1.696 kb promoter to drive expression of GFP in zebrafish retinal cells under normal conditions and after injury. Interestingly, although wild-type 1.696 kb and mutant promoters, lacking the E-box and/or HD sequences, exhibited rather similar patterns of GFP expression in the developing retina, significant differences were noticed in the mature retina. First, although the 1.696 kb promoter directed transgene expression to retinal neurons and progenitor cells, the activity of mutant promoters was drastically reduced. Second, we found that the E-box and HD sequences were necessary for transgene reinduction during optic nerve regeneration, but were not as important for transgene expression in regenerating retinal neurons after eye injury. In this latter lesion model, remarkably, both 1.696 kb and mutant promoters targeted GFP expression to Müller glia-like cells, some of which re-entered the cell cycle. These new findings will be useful for identifying the molecular signals necessary for successful CNS regeneration.

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Up-regulation of Cadherin-2 and Cadherin-4 in Regenerating Visual Structures of Adult Zebrafish

Cited by 39 publications

References 58 publications

Neurogenesis in the Fish Retina

Neurogenesis in the Fish Retina

A self-renewing division of zebrafish Müller glial cells generates neuronal progenitors that require N-cadherin to regenerate retinal neurons

An Element in the α1-Tubulin Promoter Is Necessary for Retinal Expression during Optic Nerve Regeneration But Not after Eye Injury in the Adult Zebrafish

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