Talk:Placodes

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Cite this page: Hill, M.A. (2021, January 15) Embryology Placodes. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Placodes


Entrez search - placode development

2013

Setting appropriate boundaries: Fate, patterning and competence at the neural plate border

Dev Biol. 2013 Dec 7. pii: S0012-1606(13)00644-1. doi: 10.1016/j.ydbio.2013.11.027. [Epub ahead of print]

Groves AK1, Labonne C2. Author information

Abstract

The neural crest and craniofacial placodes are two distinct progenitor populations that arise at the border of the vertebrate neural plate. This border region develops through a series of inductive interactions that begins before gastrulation and progressively divide embryonic ectoderm into neural and non-neural regions, followed by the emergence of neural crest and placodal progenitors. In this review, we describe how a limited repertoire of inductive signals-principally FGFs, Wnts and BMPs-set up domains of transcription factors in the border region which establish these progenitor territories by both cross-inhibitory and cross-autoregulatory interactions. The gradual assembly of different cohorts of transcription factors that results from these interactions is one mechanism to provide the competence to respond to inductive signals in different ways, ultimately generating the neural crest and cranial placodes. © 2013 Published by Elsevier Inc. KEYWORDS: Competence, Induction, Neural crest, Placode, Transcription factor

PMID 24321819


2012

Graded levels of Pax2a and Pax8 regulate cell differentiation during sensory placode formation

Development. 2012 Aug;139(15):2740-50. Epub 2012 Jun 28.

McCarroll MN, Lewis ZR, Culbertson MD, Martin BL, Kimelman D, Nechiporuk AV. Source Department of Cell and Developmental Biology, Oregon Health & Science University, Portland, OR 97239, USA.

Abstract

Pax gene haploinsufficiency causes a variety of congenital defects. Renal-coloboma syndrome, resulting from mutations in Pax2, is characterized by kidney hypoplasia, optic nerve malformation, and hearing loss. Although this underscores the importance of Pax gene dosage in normal development, how differential levels of these transcriptional regulators affect cell differentiation and tissue morphogenesis is still poorly understood. We show that differential levels of zebrafish Pax2a and Pax8 modulate commitment and behavior in cells that eventually contribute to the otic vesicle and epibranchial placodes. Initially, a subset of epibranchial placode precursors lie lateral to otic precursors within a single Pax2a/8-positive domain; these cells subsequently move to segregate into distinct placodes. Using lineage-tracing and ablation analyses, we show that cells in the Pax2a/8+ domain become biased towards certain fates at the beginning of somitogenesis. Experiments involving either Pax2a overexpression or partial, combinatorial Pax2a and Pax8 loss of function reveal that high levels of Pax favor otic differentiation whereas low levels increase cell numbers in epibranchial ganglia. In addition, the Fgf and Wnt signaling pathways control Pax2a expression: Fgf is necessary to induce Pax2a, whereas Wnt instructs the high levels of Pax2a that favor otic differentiation. Our studies reveal the importance of Pax levels during sensory placode formation and provide a mechanism by which these levels are controlled.

PMID 22745314

Mutual repression between Gbx2 and Otx2 in sensory placodes reveals a general mechanism for ectodermal patterning

Dev Biol. 2012 Jul 1;367(1):55-65. Epub 2012 Apr 28.

Steventon B, Mayor R, Streit A. Source Department of Craniofacial Development, King's College London, Guy's Campus, Tower Wing Floor 27, London SE1 9RT, UK. Abstract In the vertebrate head, central and peripheral components of the sensory nervous system have different embryonic origins, the neural plate and sensory placodes. This raises the question of how they develop in register to form functional sense organs and sensory circuits. Here we show that mutual repression between the homeobox transcription factors Gbx2 and Otx2 patterns the placode territory by influencing regional identity and by segregating inner ear and trigeminal progenitors. Activation of Otx2 targets is necessary for anterior olfactory, lens and trigeminal character, while Gbx2 function is required for the formation of the posterior otic placode. Thus, like in the neural plate antagonistic interaction between Otx2 and Gbx2 establishes positional information thus providing a general mechanism for rostro-caudal patterning of the ectoderm. Our findings support the idea that the Otx/Gbx boundary has an ancient evolutionary origin to which different modules were recruited to specify cells of different fates. Copyright © 2012 Elsevier Inc. All rights reserved.

PMID 22564795

2011

An effective assay for high cellular resolution time-lapse imaging of sensory placode formation and morphogenesis

BMC Neurosci. 2011 May 9;12:37.

Shiau CE, Das RM, Storey KG. Source Neural Development Group, Division of Cell & Developmental Biology, College of Life Science, University of Dundee, Dundee DD1 5EH, Scotland, UK. ceshiau@stanford.edu

Abstract

BACKGROUND: The vertebrate peripheral nervous system contains sensory neurons that arise from ectodermal placodes. Placodal cells ingress to move inside the head to form sensory neurons of the cranial ganglia. To date, however, the process of placodal cell ingression and underlying cellular behavior are poorly understood as studies have relied upon static analyses on fixed tissues. Visualizing placodal cell behavior requires an ability to distinguish the surface ectoderm from the underlying mesenchyme. This necessitates high resolution imaging along the z-plane which is difficult to accomplish in whole embryos. To address this issue, we have developed an imaging system using cranial slices that allows direct visualization of placode formation.

RESULTS: We demonstrate an effective imaging assay for capturing placode development at single cell resolution using chick embryonic tissue ex vivo. This provides the first time-lapse imaging of mitoses in the trigeminal placodal ectoderm, ingression, and intercellular contacts of placodal cells. Cell divisions with varied orientations were found in the placodal ectoderm all along the apical-basal axis. Placodal cells initially have short cytoplasmic processes during ingression as young neurons and mature over time to elaborate long axonal processes in the mesenchyme. Interestingly, the time-lapse imaging data reveal that these delaminating placodal neurons begin ingression early on from within the ectoderm, where they start to move and continue on to exit as individual or strings of neurons through common openings on the basal side of the epithelium. Furthermore, dynamic intercellular contacts are abundant among the delaminating placodal neurons, between these and the already delaminated cells, as well as among cells in the forming ganglion.

CONCLUSIONS: This new imaging assay provides a powerful method to analyze directly development of placode-derived sensory neurons and subsequent ganglia formation for the first time in amniotes. Viewing placode development in a head cross-section provides a vantage point from which it is possible to study comprehensive events in placode formation, from differentiation, cell ingression to ganglion assembly. Understanding how placodal neurons form may reveal a new mechanism of neurogenesis distinct from that in the central nervous system and provide new insight into how cells acquire motility from a stationary epithelial cell type.

PMID 2155472

http://www.biomedcentral.com/1471-2202/12/37

Includes videos of chick placodes

2010

Making senses development of vertebrate cranial placodes

Int Rev Cell Mol Biol. 2010;283:129-234.

Schlosser G. Source Zoology, School of Natural Sciences & Martin Ryan Institute, National University of Ireland, Galway, Ireland.

Abstract

Cranial placodes (which include the adenohypophyseal, olfactory, lens, otic, lateral line, profundal/trigeminal, and epibranchial placodes) give rise to many sense organs and ganglia of the vertebrate head. Recent evidence suggests that all cranial placodes may be developmentally related structures, which originate from a common panplacodal primordium at neural plate stages and use similar regulatory mechanisms to control developmental processes shared between different placodes such as neurogenesis and morphogenetic movements. After providing a brief overview of placodal diversity, the present review summarizes current evidence for the existence of a panplacodal primordium and discusses the central role of transcription factors Six1 and Eya1 in the regulation of processes shared between different placodes. Upstream signaling events and transcription factors involved in early embryonic induction and specification of the panplacodal primordium are discussed next. I then review how individual placodes arise from the panplacodal primordium and present a model of multistep placode induction. Finally, I briefly summarize recent advances concerning how placodal neurons and sensory cells are specified, and how morphogenesis of placodes (including delamination and migration of placode-derived cells and invagination) is controlled.

Copyright 2010 Elsevier Inc. All rights reserved.

PMID 20801420

The formation of the cranial ganglia by placodally-derived sensory neuronal precursors

Mol Cell Neurosci. 2010 Nov 26. Blentic A, Chambers D, Skinner A, Begbie J, Graham A.

MRC Centre for Developmental Neurobiology, King's College London, London SE1 1UL, UK. Abstract The generation of the sensory ganglia involves the migration of a precursor population to the site of ganglion formation and the differentiation of sensory neurons. There is, however, a significant difference between the ganglia of the head and trunk in that while all of the sensory neurons of the trunk are derived from the neural crest, the majority of cranial sensory neurons are generated by the neurogenic placodes. In this study, we have detailed the route through which the placodally-derived sensory neurons are generated, and we find a number of important differences between the head and trunk. Although, the neurogenic placodes release neuroblasts that migrate internally to the site of ganglion formation, we find that there are no placodally-derived progenitor cells within the forming ganglia. The cells released by the placodes differentiate during migration and contribute to the cranial ganglia as post-mitotic neurons. In the trunk, it has been shown that progenitor cells persist in the forming Dorsal Root Ganglia and that much of the process of sensory neuronal differentiation occurs within the ganglion. We also find that the period over which neuronal cells delaminate from the placodes is significantly longer than the time frame over which neural crest cells populate the DRGs. We further show that placodal sensory neuronal differentiation can occur in the absence of local cues. Finally, we find that, in contrast to neural crest cells, the different mature neurogenic placodes seem to lack plasticity. Nodose neuroblasts cannot be diverted to form trigeminal neurons and vice versa.

Copyright © 2010. Published by Elsevier Inc.

PMID: 21112397 http://www.ncbi.nlm.nih.gov/pubmed/20881354

Identification of early requirements for preplacodal ectoderm and sensory organ development

PLoS Genet. 2010 Sep 23;6(9). pii: e1001133.

Kwon HJ, Bhat N, Sweet EM, Cornell RA, Riley BB.

Biology Department, Texas A&M University, College Station, Texas, United States of America. Abstract Preplacodal ectoderm arises near the end of gastrulation as a narrow band of cells surrounding the anterior neural plate. This domain later resolves into discrete cranial placodes that, together with neural crest, produce paired sensory structures of the head. Unlike the better-characterized neural crest, little is known about early regulation of preplacodal development. Classical models of ectodermal patterning posit that preplacodal identity is specified by readout of a discrete level of Bmp signaling along a DV gradient. More recent studies indicate that Bmp-antagonists are critical for promoting preplacodal development. However, it is unclear whether Bmp-antagonists establish the proper level of Bmp signaling within a morphogen gradient or, alternatively, block Bmp altogether. To begin addressing these issues, we treated zebrafish embryos with a pharmacological inhibitor of Bmp, sometimes combined with heat shock-induction of Chordin and dominant-negative Bmp receptor, to fully block Bmp signaling at various developmental stages. We find that preplacodal development occurs in two phases with opposing Bmp requirements. Initially, Bmp is required before gastrulation to co-induce four transcription factors, Tfap2a, Tfap2c, Foxi1, and Gata3, which establish preplacodal competence throughout the nonneural ectoderm. Subsequently, Bmp must be fully blocked in late gastrulation by dorsally expressed Bmp-antagonists, together with dorsally expressed Fgf and Pdgf, to specify preplacodal identity within competent cells abutting the neural plate. Localized ventral misexpression of Fgf8 and Chordin can activate ectopic preplacodal development anywhere within the zone of competence, whereas dorsal misexpression of one or more competence factors can activate ectopic preplacodal development in the neural plate. Conversely, morpholino-knockdown of competence factors specifically ablates preplacodal development. Our work supports a relatively simple two-step model that traces regulation of preplacodal development to late blastula stage, resolves two distinct phases of Bmp dependence, and identifies the main factors required for preplacodal competence and specification.

PMID 20885782

Induction of the epibranchial placodes

http://dev.biologists.org/content/126/5/895.abstract

"The cranial sensory ganglia, in contrast to those of the trunk, have a dual embryonic origin arising from both neurogenic placodes and neural crest. Neurogenic placodes are focal thickenings of ectoderm, found exclusively in the head of vertebrate embryos. These structures can be split into two groups based on the positions that they occupy within the embryo, dorsolateral and epibranchial. The dorsolateral placodes develop alongside the central nervous system, while the epibranchial placodes are located close to the top of the clefts between the branchial arches. Importantly, previous studies have shown that the neurogenic placodes form under the influence of the surrounding cranial tissues. In this paper, we have analysed the nature of the inductive signal underlying the formation of the epibranchial placodes. We find that epibranchial placodes do not require neural crest for their induction, but rather that it is the pharyngeal endoderm that is the source of the inductive signal. We also find that, while cranial ectoderm is competent to respond to this inductive signal, trunk ectoderm is not. We have further identified the signalling molecule Bmp7 as the mediator of this inductive interaction. This molecule is expressed in a manner consistent with it playing such a role and, when added to ectoderm explants, it will promote the formation of epibranchial neuronal cells. Moreover, the Bmp7 antagonist follstatin will block the ability of pharyngeal endoderm to induce placodal neuronal cells, demonstrating that Bmp7 is required for this inductive interaction. This work answers the long standing question regarding the induction of the epibranchial placodes, and represents the first elucidation of an inductive mechanism, and a molecular effector, underlying the formation of any primary sensory neurons in higher vertebrates."


  • dorsolateral placodes - develop alongside the central nervous system
  • epibranchial placodes - located close to the top of the clefts between the branchial arches.