Mutations in laminin alpha 1 result in complex, lens-independent ocular phenotypes in zebrafish

Semina, Elena V.; Bosenko, D.V.; Zinkevich, Natalya C.; Soules, Kelly A; Hyde, David R.; Vihtelic, Thomas S.; Willer, Gregory B.; Gregg, Ronald G.; Link, Brian A.

doi:10.1016/j.ydbio.2006.07.005

Cited by 64 publications

(76 citation statements)

References 69 publications

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“…Thus, as in mammals, zebrafish lama1 is temporally regulated to be expressed broadly in early embryogenesis and down-regulated in late embryogenesis. This expression pattern overlaps with the distribution of Laminin-111, the main Laminin -containing isoform in embryos, and is consistent with defects in the development of the notochord, cerebellum and the eye in zebrafish bal mutant and conditional Lama1 knockout mice [23,[45][46][47][48][49][50]. Furthermore, the emergence of LAMA1 mutations associated with developmental defects in the cerebellum and retina in humans suggests a conversed expression pattern and function for Laminin 1 during evolution [51].…”

Section: Conservation Of Lama1 Expression Pattern In Vertebratessupporting

confidence: 64%

Hedgehog signalling acts upstream of Laminin alpha1 transcription in the zebrafish paraxial mesoderm

et al. 2017

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Section: Conservation Of Lama1 Expression Pattern In Vertebratessupporting

confidence: 64%

Hedgehog signalling acts upstream of Laminin alpha1 transcription in the zebrafish paraxial mesoderm

et al. 2017

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“…55 Interestingly, loss of the functional zebrafish homologue lama1 in ocular tissues leads to focal corneal dysplasia in adult zebrafish. 56 …”

Section: Corneal Dystrophiesmentioning

confidence: 99%

The zebrafish eye—a paradigm for investigating human ocular genetics

Richardson¹,

Tracey‐White²,

Webster

et al. 2016

Eye

147

162

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Although human epidemiological and genetic studies are essential to elucidate the aetiology of normal and aberrant ocular development, animal models have provided us with an understanding of the pathogenesis of multiple developmental ocular malformations. Zebrafish eye development displays in depth molecular complexity and stringent spatiotemporal regulation that incorporates developmental contributions of the surface ectoderm, neuroectoderm and head mesenchyme, similar to that seen in humans. For this reason, and due to its genetic tractability, external fertilisation, and early optical clarity, the zebrafish has become an invaluable vertebrate system to investigate human ocular development and disease. Recently, zebrafish have been at the leading edge of preclinical therapy development, with their amenability to genetic manipulation facilitating the generation of robust ocular disease models required for large-scale genetic and drug screening programmes. This review presents an overview of human and zebrafish ocular development, genetic methodologies employed for zebrafish mutagenesis, relevant models of ocular disease, and finally therapeutic approaches, which may have translational leads in the future.

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“…As alluded to above, proper secretion and maintenance of basement membrane proteins may be important for nuclear translocation during post-mitotic neuronal migration. Within the developing retina, transient disruptions to the entire basement membrane or specifically to laminin-1 have been shown to regulate retinal cell positioning (Halfter et al 2001;Semina et al, 2006). However, defects in basement membrane integrity in the proliferating cortex does not affect the location of M-phase, suggesting that interkinetic nuclear migration occurs normally in that region of the CNS (Haubst et al, 2006).…”

Section: Extrinsic Regulationmentioning

confidence: 99%

Nuclear migration during retinal development

2008

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In this review we focus on the mechanisms, regulation, and cellular consequences of nuclear migration in the developing retina. In the nervous system, nuclear migration is prominent during both proliferative and post-mitotic phases of development. Interkinetic nuclear migration is the process where the nucleus oscillates from the apical to basal surfaces in proliferative neuroepithelia. Proliferative nuclear movement occurs in step with the cell cycle, with M-phase being confined to the apical surface and G1-, S-, and G2-phases occurring at more basal locations. Later, following cell cycle exit, some neuron precursors migrate by nuclear translocation. In this mode of cellular migration, nuclear movement is the driving force for motility. Following discussion of the key components and important regulators for each of these processes, we present an emerging model where interkinetic nuclear migration functions to distinguish cell fates among retinal neuroepithelia. Keywordsinterkinetic nuclear migration; nuclear translocation; nucleokinesis; neurogenesis; dynein; cell cycle; cell behavior OverviewNeuronal development is regulated by a complex array of intrinsic and extrinsic signals that act on progenitor neuroepithelial cells to ensure the correct cell type is generated in the right numbers and at the appropriate time of development (Donovan et al., 2005;Cayouette et al., 2006). In addition, multiple signaling cues are integrated in post-mitotic neuronal precursors to facilitate directed cell migration and correct laminar positioning (Malicki et al., 2004). This spatial and temporal regulation of neuronal cell-type fate commitment and histogenesis is dependent on the regulation of the mitotic cell cycle, and in particular at the level of cell cycle exit (Ohnuma and Harris, 2003). Recent data suggest that nuclear migration is a critical process for several aspects of neuronal development, including that of the neural retina. The focus of this review is on interkinetic nuclear migration and nuclear translocation during retinogenesis, although much of what we know is from observations in other regions of the developing nervous system. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript Interkinetic nuclear migrationInterkinetic nuclear migration is the proliferative cell behavior where the nuclei of neuroepithelial cells migrate in an apical-basal manner and in phase with the cell cycle (Frade 2002). Neuroepithelial cell divisions are confined to apical locations while S-phase occu...

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Mutations in laminin alpha 1 result in complex, lens-independent ocular phenotypes in zebrafish

Cited by 64 publications

References 69 publications

Hedgehog signalling acts upstream of Laminin alpha1 transcription in the zebrafish paraxial mesoderm

Hedgehog signalling acts upstream of Laminin alpha1 transcription in the zebrafish paraxial mesoderm

The zebrafish eye—a paradigm for investigating human ocular genetics

Nuclear migration during retinal development

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