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

Senut, Marie Claude; Gulati-Leekha, Abhilasha; Goldman, Daniel

doi:10.1523/jneurosci.2281-04.2004

Cited by 63 publications

(75 citation statements)

References 57 publications

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“…1016␣1TIpEGFP expression vector contains 1016 bp of 5Ј flanking ␣1-tubulin DNA, exon 1, and the first intron fused in-frame to the GFP sequence. This promoter fragment is similar to the full-length 1696␣1TIpEGFP expression vector from previous work (Goldman and Ding, 2000;Goldman et al, 2001;Senut et al, 2004), except that it is lacking 680 bp from the 5Ј end. 1016␣1TIpEGFP DNA was resuspended in injection buffer, and single-cell zebrafish embryos were injected as described previously (Goldman and Ding, 2000).…”

Section: Methodsmentioning

confidence: 91%

“…Eye lesions were performed as described previously (Senut et al, 2004). Briefly, fish were anesthetized, and, under microscopic visualization, the right eye was gently pulled from its socket and stabbed four times (once in each quadrant) through the sclera with a 30 gauge needle.…”

Section: Methodsmentioning

confidence: 99%

“…Immunohistochemistry was performed as described previously (Senut et al, 2004) using the following primary antibodies: rat anti-BrdU (dividing cell marker; 1:250; Harlan Sera-Lab, Loughborough, UK); mouse zpr1 [double-cone photoreceptor marker (Larison and Bremiller, 1990); 1:250; Zebrafish International Resource Center (ZIRC), Eugene, OR]; rabbit anti-GFP (1:1000; Invitrogen, Carlsbad, CA); mouse anti-HuC/D (amacrine cell marker; 1:500; Invitrogen); rabbit anti-protein kinase C (PKC) [ON bipolar cell marker (Yazulla and Studholme, 2001); 1:250; Santa Cruz Biotechnology, Santa Cruz, CA]; mouse anti-tyrosine hydroxylase (TH) (interplexiform cell marker; 1:500; Chemicon, Temecula, CA); mouse anti-zrf1 (glial marker; 1:250; ZIRC); mouse anti-zn5 [retinal ganglion cell (RGC) marker; 1:500; ZIRC]; and mouse anti-glutamine synthetase (GS) (glial marker; 1:500; Chemicon). For BrdU immunostaining, sections were pretreated with 2N HCl for 30 min at 37°C, two 5 min rinses in 0.1 M sodium borate buffer, and three 5 min rinses in PBS, pH 7.4.…”

Section: Methodsmentioning

confidence: 99%

“…We previously demonstrated that a 1.7 kb ␣1 tubulin (␣1T) promoter fragment along with its first exon and intron directed green fluorescent protein (GFP) transgene expression to the developing and regenerating zebrafish CNS (Goldman and Ding, 2000;Goldman et al, 2001;Senut et al, 2004). In the adult CNS, this promoter directs transgene expression to neural progenitors (Goldman et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

“…In the adult CNS, this promoter directs transgene expression to neural progenitors (Goldman et al, 2001). Interestingly, retinal injury causes induction of the ␣1T promoter in a subpopulation of Müller glia that are proliferative (Senut et al, 2004;Vihtelic et al, 2006) and exhibit certain characteristics that are shared with stem cells (Yurco and Cameron, 2005). In light of these observations and because Müller glia have been reported to generate retinal neurons in other systems (Fischer and Reh, 2001;Ooto et al, 2004), we were interested in determining whether the ␣1T-expressing Müller glia function as neural progenitors in the injured zebrafish retina.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

A Role for 1 Tubulin-Expressing Muller Glia in Regeneration of the Injured Zebrafish Retina

Fausett

Goldman

2006

Journal of Neuroscience

389

555

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␣1 tubulin (␣1T) is a neuron-specific microtubule protein whose expression is induced in the developing and regenerating CNS. In the adult CNS, ␣1T expression remains high in neural progenitors. Transgenic zebrafish harboring a 1.7 kb ␣1T promoter fragment along with the first exon and intron express the transgene in a manner that recapitulates expression of the endogenous gene. We recently showed that this promoter mediates gene induction in retinal ganglion cells during optic nerve regeneration and in a subset of Müller glia that proliferate after retinal injury (Senut et al., 2004). To further characterize these Müller glia, we generated transgenic fish harboring an ␣1T promoter fragment that is specifically induced in these cells after retinal damage. Transgene expression, bromodeoxyuridine (BrdU) labeling, and stem cell marker expression suggested that ␣1T-expressing Müller glia dedifferentiate and become multipotent in response to injury. In addition, green fluorescent protein and BrdU-mediated lineage tracing combined with retinal gene expression analysis indicated that ␣1T-expressing Müller glia were capable of generating retinal neurons and glia. These data strongly suggest ␣1T-expressing Müller glia dedifferentiate and mediate regeneration of the injured zebrafish retina.

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Section: Methodsmentioning

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A Role for 1 Tubulin-Expressing Muller Glia in Regeneration of the Injured Zebrafish Retina

Fausett

Goldman

2006

Journal of Neuroscience

389

555

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Zebrafish as a Model System for Successful Spinal Cord Regeneration

Becker

2006

Model Organisms in Spinal Cord Regeneration

101

114

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OverviewAdult zebrafish, in contrast to mammals, are capable of functional regeneration after spinal cord injury. Regeneration studies in zebrafish benefit from the model status of this vertebrate for research on developmental biology. This model status has helped to make available molecular tools such as genetic manipulation, expression profiling and gene knock-down techniques. Behavioral recovery after spinal injury is clearly quantifiable in zebrafish using different tests. The anatomical basis for behavioral recovery is supported by a surprising heterogeneity in axon regrowth and gene expression in different neuronal populations. In addition, specific gene regulation in non-axotomized spinal neurons indicates plasticity of the spinal circuitry after injury, which may also contribute to behavioral recovery. Gaps in our understanding of the spinal network are being filled by several studies of the more simple spinal network found in larval zebrafish. Gene knock-down, interference with intracellular messenger systems and promoter analysis in neurons after lesion are all possible in vivo, demonstrating the experimental accessibility of the system. At the same time, environmental inhibitors of axon re-growth appear not to be prominent in fish. Thus, environmental conditions may not confound the study of neuronal reactions to axotomy. Zebrafish, therefore, offer the opportunity to perform in-vivo studies of the mechanisms that lead to successful recovery after spinal cord injury, from the molecular to the systems levels.

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An insight on established retinal injury mechanisms and prevalent retinal stem cell activation pathways in vertebrate models

Sherpa

Hui

2021

Anim Models and Exp Med

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The brain processes visual information when light energy transduces into neural activity in the retina. The close-knit components of the central nervous system (CNS), the brain, and its extension retina are thus the critical players in visual perception, thereby aiding in daily activities. While the brain remains well protected inside the skull, the eyes are quite susceptible to physical injuries and chemical accidents. 1 Furthermore, one's genetic makeup and increasing age also invite multiple numbers of eye diseases such as retinitis pigmentosa (RP), age-related macular degeneration (AMD), glaucoma, etc All this has contributed to the recent "World Reports on vision (2019)," which shows that a whopping 2.2 billion people globally fell victim to visual impairment in the past year. 2 The discovery of the existence of adult retinal stem/progenitor cells among different vertebrate species 3 and its high reparative activity in the case of lower vertebrates has presented us with a possibility to "self-heal" the retina one day. 4 Consequently, high regeneration competent animals, which include the amphibian newts and Xenopus, teleost zebrafish (Danio rerio), and chick are thus being explored 5 to investigate different genetic and epigenetic features, signaling pathways, and factors 6,7 that regulate stem cell activation, thus gradually filling in the gaps of our knowledge of mammals, which appear to be the least competent among the group. 8 With the hope of updating and giving researchers an idea about how these animal models have significantly shaped our understanding of the retinal regeneration process, in this review,

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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

Cited by 63 publications

References 57 publications

A Role for 1 Tubulin-Expressing Muller Glia in Regeneration of the Injured Zebrafish Retina

A Role for 1 Tubulin-Expressing Muller Glia in Regeneration of the Injured Zebrafish Retina

Zebrafish as a Model System for Successful Spinal Cord Regeneration

An insight on established retinal injury mechanisms and prevalent retinal stem cell activation pathways in vertebrate models

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