Cadherin-2 participates in the morphogenesis of the zebrafish inner ear

Clendenon, Sherry G.; Shen, Yu Chi; Liu, Qin; Turner, Katharyn E.; Mills, Mark C.; Cook, Greg W.; Miller, Caroline; Gattone, Vincent H.; Barald, Kate F.; Marrs, James A.

doi:10.1242/jcs.03299

Cited by 20 publications

(17 citation statements)

References 56 publications

(62 reference statements)

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“…In dfna5 morphants and jekyll ( ugdh ) mutants, HA fails to be produced, and projection outgrowth is blocked (Neuhauss et al, 1996; Busch-Nentwich et al, 2004). Variable projection outgrowth defects in the zebrafish ear have also been reported after knockdown or mutation of ncs1a (Blasiole et al, 2005), atrophin2 ( rerea - Zebrafish Information Network), fgf8a (Asai et al, 2006), cdh2 (Babb-Clendenon et al, 2006), atp1a1a.2 (Blasiole et al, 2006), atp2b1a (Cruz et al, 2009) and grhl2 (Han et al, 2011), and in Hedgehog pathway mutants (Hammond et al, 2010). …”

Section: Introductionmentioning

confidence: 93%

Semicircular canal morphogenesis in the zebrafish inner ear requires the function ofgpr126(lauscher), an adhesion class G protein-coupled receptor gene

et al. 2013

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Morphogenesis of the semicircular canal ducts in the vertebrate inner ear is a dramatic example of epithelial remodelling in the embryo, and failure of normal canal development results in vestibular dysfunction. In zebrafish and Xenopus, semicircular canal ducts develop when projections of epithelium, driven by extracellular matrix production, push into the otic vesicle and fuse to form pillars. We show that in the zebrafish, extracellular matrix gene expression is high during projection outgrowth and then rapidly downregulated after fusion. Enzymatic disruption of hyaluronan in the projections leads to their collapse and a failure to form pillars: as a result, the ears swell. We have cloned a zebrafish mutant, lauscher (lau), identified by its swollen ear phenotype. The primary defect in the ear is abnormal projection outgrowth and a failure of fusion to form the semicircular canal pillars. Otic expression of extracellular matrix components is highly disrupted: several genes fail to become downregulated and remain expressed at abnormally high levels into late larval stages. The lau mutations disrupt gpr126, an adhesion class G protein-coupled receptor gene. Expression of gpr126 is similar to that of sox10, an ear and neural crest marker, and is partially dependent on sox10 activity. Fusion of canal projections and downregulation of otic versican expression in a hypomorphic lau allele can be restored by cAMP agonists. We propose that Gpr126 acts through a cAMP-mediated pathway to control the outgrowth and adhesion of canal projections in the zebrafish ear via the regulation of extracellular matrix gene expression.

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Section: Introductionmentioning

confidence: 93%

Semicircular canal morphogenesis in the zebrafish inner ear requires the function ofgpr126(lauscher), an adhesion class G protein-coupled receptor gene

et al. 2013

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“…Nevertheless, it remains unclear whether ß-catenin plays a direct role in placode cell delamination. Several important molecules, such as ephrins, integrins, tetraspanins, and cadherins, have all been implicated in signaling and cell adhesion, and in the delamination process (Babb-Clendenon et al, 2006; Davies, 2007; Hong et al, 2012; McCabe and Bronner, 2011; Saeger et al, 2011). Their role in neural crest cell EMT and migration has been studied significantly (Kerosuo and Bronner-Fraser, 2012) more than in the placodes, where the most comprehensive works on placode cell delamination are primarily descriptive (Graham et al, 2007; Shiau et al, 2011).…”

Section: Conclusion and Prospectivementioning

confidence: 99%

Signaling mechanisms controlling cranial placode neurogenesis and delamination

Lassiter

Stark

Zhao

et al. 2014

Developmental Biology

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The neurogenic cranial placodes are a unique transient epithelial niche of neural progenitor cells that give rise to multiple derivatives of the peripheral nervous system, particularly, the sensory neurons. Placode neurogenesis occurs throughout an extended period of time with epithelial cells continually recruited as neural progenitor cells. Sensory neuron development in the trigeminal, epibranchial, otic, and olfactory placodes coincides with detachment of these neuroblasts from the encompassing epithelial sheet, leading to delamination and ingression into the mesenchyme where they continue to differentiate as neurons. Multiple signaling pathways are known to direct placodal development. This review defines the signaling pathways working at the finite spatiotemporal period when neuronal selection within the placodes occurs, and neuroblasts concomitantly delaminate from the epithelium. Examining neurogenesis and delamination after initial placodal patterning and specification has revealed a common trend throughout the neurogenic placodes, which suggests that both activated FGF and attenuated Notch signaling activities are required for neurogenesis and changes in epithelial cell adhesion leading to delamination. We also address the varying roles of other pathways such as the Wnt and BMP signaling families during sensory neurogenesis and neuroblast delamination in the differing placodes.

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“…The observed loss of columnar morphology of the otic vesicle epithelium coupled with a decrease in the levels of the junction markers ␣-catenin, vinculin and occludin further supports this model. Loss of cadherin-2, a component of adherens junctions, also results in reduced otic vesicle size (Babb-Clendenon et al, 2006), underscoring the importance of cellular adhesions in otic vesicle morphogenesis.…”

Section: Epithelial Integrity Of the Otic Vesicle Is Regulated By Xevlmentioning

confidence: 95%

Regulation of otic vesicle and hair cell stereocilia morphogenesis by Ena/VASP-like (Evl) inXenopus

Wanner

Miller

2007

Journal of Cell Science

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The inner ear is derived from a thickening in the embryonic ectoderm, called the otic placode. This structure undergoes extensive morphogenetic movements throughout its development and gives rise to all components of the inner ear. Ena/VASP-like (Evl) is an actin binding protein involved in the regulation of cytoskeletal dynamics and organization. We have examined the role of Evl during the morphogenesis of the Xenopus inner ear. Evl (hereafter referred to as Xevl) is expressed throughout otic vesicle formation and is enriched in the neuroblasts that delaminate to form the vestibulocochlear ganglion and in hair cells that possess mechanosensory stereocilia. Knockdown of Xevl perturbs epithelial morphology and intercellular adhesion in the otic vesicle and disrupts formation of the vestibulocochlear ganglion, evidenced by reduction of ganglion size, disorganization of the ganglion, and defects in neurite outgrowth. Later in embryogenesis, Xevl is required for development of mechanosensory hair cells. In Xevl knockdown embryos, hair cells of the ventromedial sensory epithelium display multiple abnormalities including disruption of the cuticular plate at the base of stereocilia and disorganization of the normal staircase appearance of stereocilia. Based on these data, we propose that Xevl plays an integral role in regulating morphogenesis of the inner ear epithelium and the subsequent development of the vestibulocochlear ganglion and mechanosensory hair cells.

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Cadherin-2 participates in the morphogenesis of the zebrafish inner ear

Cited by 20 publications

References 56 publications

Semicircular canal morphogenesis in the zebrafish inner ear requires the function ofgpr126(lauscher), an adhesion class G protein-coupled receptor gene

Semicircular canal morphogenesis in the zebrafish inner ear requires the function ofgpr126(lauscher), an adhesion class G protein-coupled receptor gene

Signaling mechanisms controlling cranial placode neurogenesis and delamination

Regulation of otic vesicle and hair cell stereocilia morphogenesis by Ena/VASP-like (Evl) inXenopus

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