Cellular commitment and differentiation in the organ of Corti

Kelley, Matthew W.

doi:10.1387/ijdb.072388mk

Cited by 88 publications

(97 citation statements)

References 117 publications

(143 reference statements)

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“…This correlates with the fact that mutations of SOX2 in humans cause sensorineural hearing loss (Hagstrom et al, 2005). These data show that proneural basic Helix-Loop-Helix genes require this prepatterning event to function (Kelley, 2007) In the late seventies, proneural genes were associated with a gene complex (García-Bellido, 1979) and the genetic and molecular analysis of the achaete-scute complex (ASC) in flies lead to the identification of four genes in the complex, whose vertebrate counterparts were unveiled during the nineties (Ghysen and Dambly-Chaudiere, 2000;Bertrand et al, 2002). A further Drosophila proneural gene, atonal, was isolated later in a PCR-based screen to identify bHLH sequences and the orthologs of this gene subfamily have been shown by loss-of-function analysis to be critical for ear development (see Jarman, 1993; Bermingham et al, 1999;Kim et al, 2001;Ma et al, 1998).…”

supporting

confidence: 63%

“…While this can be crudely demonstrated in appropriate null mutants, the biologically relevant molecular interplay in the undisturbed cell will be far more complex as indicated by the work of Segil and Pirvola (Mantela et al, 2005, White et al, 2006. Our current understanding of certain aspects of this process is reviewed here by RochaSanchez (2007) and how this relates to differentiation is discussed by Kelley (2007). Clearly, full understanding of cell cycle regulation with molecular tools to safely start and stop this would be beneficial for any strategy to restore hearing loss.…”

Section: Cell Cycle Cell Determination and Differentiationmentioning

confidence: 99%

“…One preliminary but useful scheme of the possible sequence of cell fate decisions from an early multipotent progenitor to the different cell types was also proposed by Donna Fekete in a short review that became a classic (Fekete, 1996). By then, the discovery by Doris Wu that there were genes that foreshadowed the generation of sensory patches (Wu & Oh, 1966;Oh et al, 1966) and the cloning of the vertebrate homologues of Notch, Delta and Serrate genes (Henrique, 1995;Myat, 1996) lead to the current view on neuron and hair cell specification: the specification of an epithelial domain with neuro-sensory competence that gives rise to the neurons and hair cells through a mechanism of proneural gene mediated specification, which is enhanced by lateral inhibition (Cole et al, 2000;Alsina et al, 2003; Sanchez-Calderón et al, 2007;Kelley, 2007).…”

mentioning

confidence: 99%

“…It is now clear that Neurog1, NeuroD1 and Atoh1 are at the core of the proneural bHLH function in the ear. They are necessary and sufficient to promote neuronal and hair cell fates, respectively Woods et al, 2004) and are reviewed in this issue by Kelley, 2007 andSanchez-Calderón, et al, 2007). NeuroD1 behaves as a neuronal differentiation gene that acts after Neurog1 and Atoh1 is a proneural gene that confers a prosensory cell cluster with competence to develop into hair-and supporting cells.…”

mentioning

confidence: 99%

“…Finally, ectopic expression of Atoh1 induces sensory cells of mixed hair cell-supporting cell phenotypes (Raphael, 2007 in this volume), which suggests that factors other than Atoh1 may be needed to fully de-differentiate supporting cells in a regeneration paradiam. (Liu et al, 2006;Kelley, 2007).…”

mentioning

confidence: 99%

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The molecular biology of ear development - "Twenty years are nothing"

Giráldez

Fritzsch²

2007

Int. J. Dev. Biol.

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Views of classical biological problems changed dramatically with the rise of molecular biology as a common framework. It was indeed the new language of life sciences. Molecular biology increasingly moved us towards a unified view of developmental genetics as ideas and techniques were imported to vertebrates from other biological systems where genetics was in a more advanced state. The ultimate advance has been the ability to actually perform genetic manipulations in vertebrate organisms that were almost unthinkable before. During the last two decades these technical advances entered into and affected the research on ear development. These events are still very recent and have been with us for no longer than two decades, which is the reason for the title of this article. This new scenario forms the basis of the current and productive work of many laboratories, and this is what this Special Issue of The International Journal of Developmental Biology wants to show, presenting a snapshot of insights at the beginning of the 21st Century. In this article, we give an overview of the topics that are addressed in this Ear Development Special Issue, and also we take the opportunity to informally dig into the genealogy of some of those topics, trying to link the current work with some classical work of the past. KEY WORDS: cell fate, patterning, hair cell, otic neuron, morphogenesis, evolution, regenerationEach time is characterised by the field of possibility that defines not only the standing theories or beliefs, but also the nature of the objects which are accessible to analysis, the means to look at them and the way to observe and to talk about them. (Jacob, 1976) There has been a sustained interest in ear developmental biology all throughout the 20 th century. As with many other fields in biology and neurosciences, this interest is in part rooted in curiosity and in part is driven by the intent to understand and cure diseases. There is an immense catalogue of histological observations and clever experimental manipulations of the embryonic ear that have contributed to an increase in our knowledge of the development of the ear and that was able to paint a picture of ear development by the end of the eighties (see Rubel, 1978; and the report of the Holte Symposium (Cremers et al., 1987). The view at the end of the eighties, however detailed, remained descriptive and phenomenological: the gap between cells, genes and proteins was Int. J. Dev. Biol. 51: 429-438 (2007) still too large and many processes were unknown leaving "the widest gap to be filled… to understanding how cells with identical genomes may become differentiated" (Jacob, 1947). Thirty years elapsed from the publishing of the double helix in 1953 to the polymerase chain reaction (Saiki et al., 1985) and during this period of time the whole of biology was changed and set a new paradigm. Views of classical biological problems, changed dramatically with the rise of molecular biology as a common framework. It was indeed the new language of life scien...

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supporting

confidence: 63%

Section: Cell Cycle Cell Determination and Differentiationmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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The molecular biology of ear development - "Twenty years are nothing"

Giráldez

Fritzsch²

2007

Int. J. Dev. Biol.

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Early Development of the Vertebrate Inner Ear

Magariños

Contreras

Aburto

et al. 2012

The Anatomical Record

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This is a review of the biological processes and the main signaling pathways required to generate the different otic cell types, with particular emphasis on the actions of insulin-like growth factor I. The sensory organs responsible of hearing and balance have a common embryonic origin in the otic placode. Lineages of neural, sensory, and support cells are generated from common otic neuroepithelial progenitors. The sequential generation of the cell types that will form the adult inner ear requires the coordination of cell proliferation with cell differentiation programs, the strict regulation of cell survival, and the metabolic homeostasis of otic precursors. A network of intracellular signals operates to coordinate the transcriptional response to the extracellular input. Understanding the molecular clues that direct otic development is fundamental for the design of novel treatments for the protection and repair of hearing loss and balance disorders.

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An in vitro mouse model of congenital cytomegalovirus‐induced pathogenesis of the inner ear cochlea

Melnick

Jaskoll

2012

Birth Defects Research

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Congenital human cytomegalovirus (CMV) infection is the leading nongenetic etiology of sensorineural hearing loss (SNHL) at birth and prelingual SNHL not expressed at birth. The paucity of temporal bone autopsy specimens from infants with congenital CMV infection has hindered the critical correlation of histopathology with pathogenesis. Here, we present an in vitro embryonic mouse model of CMV-infected cochleas that mimics the human sites of viral infection and associated pathology. There is a striking dysplasia/hyperplasia in mouse CMV-infected cochlear epithelium and mesenchyme, including organ of Corti hair and supporting cells and stria vascularis. This is concomitant with significant dysregulation of p19, p21, p27, and Pcna gene expression, as well as proliferating cell nuclear antigen (PCNA) protein expression. Other pathologies similar to those arising from known deafness gene mutations include downregulation of KCNQ1 protein expression in the stria vascularis, as well as hypoplastic and dysmorphic melanocytes. Thus, this model provides a relevant and reliable platform within which the detailed cell and molecular biology of CMV-induced deafness may be studied.

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Cellular commitment and differentiation in the organ of Corti

Cited by 88 publications

References 117 publications

The molecular biology of ear development - "Twenty years are nothing"

The molecular biology of ear development - "Twenty years are nothing"

Early Development of the Vertebrate Inner Ear

An in vitro mouse model of congenital cytomegalovirus‐induced pathogenesis of the inner ear cochlea

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