The expression of NOTCH2, HES1 and SOX9 during mouse retinal development

Zhu, Minyan; Gasperowicz, Malgorzata; Chow, Robert L.

doi:10.1016/j.gep.2012.12.001

Cited by 24 publications

(21 citation statements)

References 25 publications

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“…Localization at the apical surface of the neuroepithelium (diencephalon and RPE) was also evident. Some retinal and RPE cells expressing Yap also expressed Sox9, a gene essential for RPE and retina development (Masuda et al, 2014; Poche et al, 2008; Zhu et al, 2013). At OC stages, Yap was expressed in most developing ocular tissues of the OC, lens, retina, CB and iris primordia, RPE, cornea, extraocular muscles and periocular mesenchymal cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

Yap is essential for retinal progenitor cell cycle progression and RPE cell fate acquisition in the developing mouse eye

Kim

Park

Lee

et al. 2016

Developmental Biology

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Yap functions as a transcriptional regulator by acting together with sequence-specific DNA binding factors and transcription cofactors to mediate cell proliferation in developing epithelial tissues and tumors. An upstream kinase cascade controls nuclear localization and function in response to partially identified exogenous signals, including cell-to-cell contact. Nevertheless, its role in CNS development is poorly understood. In order to investigate Yap function in developing CNS, we characterized the cellular outcomes after selective Yap gene ablation in developing ocular tissues. When Yap was lost, presumptive retinal pigment epithelium acquired anatomical and molecular characteristics resembling those of the retinal epithelium rather than of RPE, including loss of pigmentation, pseudostratified epithelial morphology and ectopic induction of markers for retinal progenitor cells, like Chx10, and neurons, like β-Tubulin III. In addition, developing retina showed signs of progressive degeneration, including laminar folding, thinning and cell loss, which resulted from multiple defects in cell proliferation and survival, and in junction integrity. Furthermore, Yap-deficient retinal progenitors displayed decreased S-phase cells and altered cell cycle progression. Altogether, our studies not only illustrate the canonical function of Yap in promoting the proliferation of progenitors, but also shed new light on its evolutionarily conserved, instructive role in regional specification, maintenance of junctional integrity and precise regulation of cell proliferation during neuroepithelial development.

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Section: Resultsmentioning

confidence: 99%

Yap is essential for retinal progenitor cell cycle progression and RPE cell fate acquisition in the developing mouse eye

Kim

Park

Lee

et al. 2016

Developmental Biology

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“…One possibility is that, as in other tissues, ALK is involved in the midkine-induced proliferation (Reiff et al, 2011). Also, a recent study has shown that in the developing mouse retina, notch2 is expressed in progenitors and Müller glia (Zhu et al, 2013), an expression pattern that is reminiscent of that for mdka in the developing zebrafish. In addition, in zebrafish the cellular expression of mdka and notch2 are similar during retinal regeneration (Cameron et al, 2005;Calinescu et al, 2009a).…”

Section: Midkine Receptors In the Retinamentioning

confidence: 99%

“…Neural layer of E11.5 and E13.5 mouse retina Vernersson et al, 2006. Notch2 Mouse Müller glia Roesch et al, 2008; Mouse E9.5 optical vesicle, E11.5 and E14.5 retinal progenitors, presumptive future Müller glial cells at P6, adult Müller glia Zhu et al, 2013; Weak expression in adult zebrafish retina but up-regulated after lesion Cameron et al, 2005.…”

Section: Alkmentioning

confidence: 99%

The expression and function of midkine in the vertebrate retina

Gramage

Hitchcock

2014

British J Pharmacology

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The functional role of midkine during development, following injury and in disease has been studied in a variety of tissues. In this review, we summarize what is known about midkine in the vertebrate retina, focusing largely on recent studies utilizing the zebrafish (Danio rerio) as an animal model. Zebrafish are a valuable animal model for studying the retina, due to its very rapid development and amazing ability for functional neuronal regeneration following neuronal cell death. The zebrafish genome harbours two midkine paralogues, midkine-a (mdka) and midkine-b (mdkb), which, during development, are expressed in nested patterns among different cell types. mdka is expressed in the retinal progenitors and mdkb is expressed in newly post-mitotic cells. Interestingly, studies of loss- and gain-of-function in zebrafish larvae indicate that midkine-a regulates cell cycle kinetics. Moreover, both mdka and mdkb are expressed in different cell types in the normal adult zebrafish retina, but after light-induced death of photoreceptors, both are up-regulated and expressed in proliferating Müller glia and photoreceptor progenitors, suggesting an important and (perhaps) coincident role for these cytokines during stem cell-based neuronal regeneration. Based on its known role in other tissues and the expression and function of the midkine paralogues in the zebrafish retina, we propose that midkine has an important functional role both during development and regeneration in the retina. Further studies are needed to understand this role and the mechanisms that underlie it.

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“…Our data demonstrate that the slincR transcript functions as an RNA macromolecule and acts locally (in cis ) on chromosome 3 to regulate the spatial and relative expression levels of sox9b . We detected slincR expression in tissues that have reported essential functions for sox9 , including the otic vesicle, eye, and brain (Yan et al, 2005; Scott et al, 2010; Zhu et al, 2013). Upon TCDD exposure, sox9b expression is reduced in zebrafish heart ventricles (Hofsteen et al, 2013).…”

Section: Discussionmentioning

confidence: 96%

“…Evidence from mouse chondrogenic ATDC5 cells suggests that notch signaling initially induces Sox9 expression, but prolonged notch signaling leads to suppression of Sox9 transcription via secondary effectors (Chen et al, 2013). Notch signaling in ectoderm-derived cells, which includes the central nervous system, otic placode, and eye, was shown to induce sox9 expression for stem cell maintenance, astrogliogenesis, and eye development (Martini et al, 2013; Zhu et al, 2013). …”

Section: Discussionmentioning

confidence: 99%

In Vivo Characterization of an AHR-Dependent Long Noncoding RNA Required for Proper Sox9b Expression

et al. 2017

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Xenobiotic activation of the aryl hydrocarbon receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the proper formation of craniofacial cartilage and the heart in developing zebrafish. Downstream molecular targets responsible for AHR-dependent adverse effects remain largely unknown; however, in zebrafish sox9b has been identified as one of the most-reduced transcripts in several target organs and is hypothesized to have a causal role in TCDD-induced toxicity. The reduction of sox9b expression in TCDD-exposed zebrafish embryos has been shown to contribute to heart and jaw malformation phenotypes. The mechanisms by which AHR2 (functional ortholog of mammalian AHR) activation leads to reduced sox9b expression levels and subsequent target organ toxicity are unknown. We have identified a novel long noncoding RNA (slincR) that is upregulated by strong AHR ligands and is located adjacent to the sox9b gene. We hypothesize that slincR is regulated by AHR2 and transcriptionally represses sox9b. The slincR transcript functions as an RNA macromolecule, and slincR expression is AHR2 dependent. Antisense knockdown of slincR results in an increase in sox9b expression during both normal development and AHR2 activation, which suggests relief in repression. During development, slincR was expressed in tissues with sox9 essential functions, including the jaw/snout region, otic vesicle, eye, and brain. Reducing the levels of slincR resulted in altered neurologic and/or locomotor behavioral responses. Our results place slincR as an intermediate between AHR2 activation and the reduction of sox9b mRNA in the AHR2 signaling pathway.

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The expression of NOTCH2, HES1 and SOX9 during mouse retinal development

Cited by 24 publications

References 25 publications

Yap is essential for retinal progenitor cell cycle progression and RPE cell fate acquisition in the developing mouse eye

Yap is essential for retinal progenitor cell cycle progression and RPE cell fate acquisition in the developing mouse eye

The expression and function of midkine in the vertebrate retina

In Vivo Characterization of an AHR-Dependent Long Noncoding RNA Required for Proper Sox9b Expression

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