The Experts below are selected from a list of 381 Experts worldwide ranked by ideXlab platform

Jo Begbie - One of the best experts on this subject based on the ideXlab platform.

  • Identification of molecular signatures specific for distinct cranial sensory ganglia in the developing chick
    Neural Development, 2016
    Co-Authors: Cedric Patthey, Harry Clifford, Wilfried Haerty, Chris P. Ponting, Sebastian M. Shimeld, Jo Begbie
    Abstract:

    Background The cranial sensory ganglia represent populations of neurons with distinct functions, or sensory modalities. The production of individual ganglia from distinct Neurogenic Placodes with different developmental pathways provides a powerful model to investigate the acquisition of specific sensory modalities. To date there is a limited range of gene markers available to examine the molecular pathways underlying this process. Results Transcriptional profiles were generated for populations of differentiated neurons purified from distinct cranial sensory ganglia using microdissection in embryonic chicken followed by FAC-sorting and RNAseq. Whole transcriptome analysis confirmed the division into somato- versus viscerosensory neurons, with additional evidence for subdivision of the somatic class into general and special somatosensory neurons. Cross-comparison of distinct ganglia transcriptomes identified a total of 134 markers, 113 of which are novel, which can be used to distinguish trigeminal, vestibulo-acoustic and epibranchial neuronal populations. In situ hybridisation analysis provided validation for 20/26 tested markers, and showed related expression in the target region of the hindbrain in many cases. Conclusions One hundred thirty-four high-confidence markers have been identified for placode-derived cranial sensory ganglia which can now be used to address the acquisition of specific cranial sensory modalities.

  • Migration of Neuroblasts from Neurogenic Placodes
    Developmental Neuroscience, 2007
    Co-Authors: Jo Begbie
    Abstract:

    Peripheral neurons involved in cephalic sensory systems are born in the ectoderm at a distance from the neural tube. The neuroblasts migrate internally, coalesce to form ganglia and extend axons to th

  • delamination of cells from Neurogenic Placodes does not involve an epithelial to mesenchymal transition
    Development, 2007
    Co-Authors: Anthony Graham, Aida Blentic, Sandra Duque, Jo Begbie
    Abstract:

    Neurogenic Placodes are specialized regions of embryonic ectoderm that generate the majority of the neurons of the cranial sensory ganglia. Here we examine in chick the mechanism underlying the delamination of cells from the epibranchial placodal ectoderm. We show that the placodal epithelium has a distinctive morphology, reflecting a change in cell shape, and is associated with a breach in the underlying basal lamina. Placodal cell delamination is distinct from neural crest cell delamination. In particular, exit of neuroblasts from the epithelium is not associated with the expression of Snail/Snail2 or of the Rho family GTPases required for the epithelial-to-mesenchymal transition seen in neural crest cell delamination. Indeed, cells leaving the Placodes do not assume a mesenchymal morphology but migrate from the epithelium as neuronal cells. We further show that the placodal epithelium has a pseudostratified appearance. Examination of proliferation shows that the placodal epithelium is mitotically quiescent, with few phosphohistone H3-positive cells being identified. Where division does occur within the epithelium it is restricted to the apical surface. The Neurogenic Placodes thus represent specialized ectodermal niches that generate neuroblasts over a protracted period.

  • Neurogenic Placodes: a common front
    Trends in neurosciences, 2000
    Co-Authors: Anthony Graham, Jo Begbie
    Abstract:

    Abstract Neurogenic Placodes are specialized regions of the embryonic ectoderm that are central to the development of the cranial sensory systems of vertebrates. These structures generate many of the sensory neurones of the head and also, in some instances, the associated sensory receptor cells. The Neurogenic Placodes have often been thought to share common pathways of development and to have evolved together. However, recent work has shown that this is not the case. The term ‘Neurogenic Placodes' no longer seems to describe a cohesive group. Rather, the Neurogenic Placodes fall into a number of categories, and it is within each of these that the members share a common development and evolution.

Clare V.h. Baker - One of the best experts on this subject based on the ideXlab platform.

  • a fate map for cranial sensory ganglia in the sea lamprey
    Developmental Biology, 2014
    Co-Authors: Melinda S Modrell, Marianne E. Bronner, Tatjana Saukaspengler, Dorit Hockman, David Buckley, Clare V.h. Baker
    Abstract:

    Cranial Neurogenic Placodes and the neural crest make essential contributions to key adult characteristics of all vertebrates, including the paired peripheral sense organs and craniofacial skeleton. Neurogenic placode development has been extensively characterized in representative jawed vertebrates (gnathostomes) but not in jawless fishes (agnathans). Here, we use in vivo lineage tracing with DiI, together with neuronal differentiation markers, to establish the first detailed fate-map for placode-derived sensory neurons in a jawless fish, the sea lamprey Petromyzon marinus, and to confirm that neural crest cells in the lamprey contribute to the cranial sensory ganglia. We also show that a pan-Pax3/7 antibody labels ophthalmic trigeminal (opV, profundal) placode-derived but not maxillomandibular trigeminal (mmV) placode-derived neurons, mirroring the expression of gnathostome Pax3 and suggesting that Pax3 (and its single Pax3/7 lamprey ortholog) is a pan-vertebrate marker for opV placode-derived neurons. Unexpectedly, however, our data reveal that mmV neuron precursors are located in two separate domains at neurula stages, with opV neuron precursors sandwiched between them. The different branches of the mmV nerve are not comparable between lampreys and gnatho-stomes, and spatial segregation of mmV neuron precursor territories may be a derived feature of lampreys. Nevertheless, maxillary and mandibular neurons are spatially segregated within gnathostome mmV ganglia, suggesting that a more detailed investigation of gnathostome mmV placode development would be worthwhile. Overall, however, our results highlight the conservation of cranial peripheral sensory nervous system development across vertebrates, yielding insight into ancestral vertebrate traits.

  • Activation of Pax3 target genes is necessary but not sufficient for neurogenesis in the ophthalmic trigeminal placode.
    Developmental biology, 2008
    Co-Authors: Carolynn M. Dude, Frederic Relaix, C.-y. Kelly Kuan, James R. Bradshaw, Nicholas D. E. Greene, Michael R. Stark, Clare V.h. Baker
    Abstract:

    Abstract Vertebrate cranial Neurogenic Placodes are relatively simple model systems for investigating the control of sensory neurogenesis. The ophthalmic trigeminal (opV) placode, for which the earliest specific marker is the paired domain homeodomain transcription factor Pax3, forms cutaneous sensory neurons in the ophthalmic lobe of the trigeminal ganglion. We previously showed that Pax3 expression in avian opV placode cells correlates with specification and commitment to a Pax3+, cutaneous sensory neuron fate. Pax3 can act as a transcriptional activator or repressor, depending on the cellular context. We show using mouse Splotch2H mutants that Pax3 is necessary for the normal neuronal differentiation of opV placode cells. Using an electroporation construct encoding a Pax3–Engrailed fusion protein, which represses Pax3 target genes, we show that activation of Pax3 target genes is required cell-autonomously within chick opV placode cells for expression of the opV placode markers FGFR4 and Ngn2, maintenance of the preplacodal marker Eya2, expression of Pax3 itself (suggesting that Pax3 autoregulates), neuronal differentiation and delamination. Mis-expression of Pax3 in head ectoderm is sufficient to induce FGFR4 and Ngn2 expression, but neurons do not differentiate, suggesting that additional signals are necessary to enable Pax3+ cells to differentiate as neurons. Mis-expression of Pax3 in the Pax2+ otic and epibranchial Placodes also downregulates Pax2 and disrupts otic vesicle closure, suggesting that Pax3 is sufficient to alter the identity of these cells. Overall, our results suggest that activation of Pax3 target genes is necessary but not sufficient for neurogenesis in the opV placode.

  • A molecular analysis of Neurogenic placode and cranial sensory ganglion development in the shark, Scyliorhinus canicula.
    Developmental biology, 2006
    Co-Authors: Paul O'neill, Ruth B. Mccole, Clare V.h. Baker
    Abstract:

    In order to gain insight into the evolution of the genetic control of the development of cranial Neurogenic Placodes and cranial sensory ganglia in vertebrates, we cloned and analysed the spatiotemporal expression pattern of six transcription factor genes in a chondrichthyan, the shark Scyliorhinus canicula (lesser-spotted dogfish/catshark). As in other vertebrates, NeuroD is expressed in all cranial sensory ganglia. We show that Pax3 is expressed in the profundal placode and ganglion, strongly supporting homology between the separate profundal ganglion of elasmobranchs and basal actinopterygians and the ophthalmic trigeminal placode-derived neurons of the fused amniote trigeminal ganglion. We show that Pax2 is a conserved pan-gnathostome marker for epibranchial and otic Placodes, and confirm that Phox2b is a conserved pan-gnathostome marker for epibranchial placode-derived neurons. We identify Eya4 as a novel marker for the lateral line system throughout its development, expressed in lateral line Placodes, sensory ridges and migrating primordia, neuromasts and electroreceptors. We also identify Tbx3 as a specific marker for lateral line ganglia in shark embryos. We use the spatiotemporal expression pattern of these genes to characterise the development of Neurogenic Placodes and cranial sensory ganglia in the dogfish, with a focus on the epibranchial and lateral line Placodes. Our findings demonstrate the evolutionary conservation across all gnathostomes of at least some of the transcription factor networks underlying Neurogenic placode development.

  • establishing neuronal identity in vertebrate Neurogenic Placodes
    Development, 2000
    Co-Authors: Clare V.h. Baker, Marianne Bronnerfraser
    Abstract:

    The trigeminal and epibranchial Placodes of vertebrate embryos form different types of sensory neurons. The trigeminal Placodes form cutaneous sensory neurons that innervate the face and jaws, while the epibranchial Placodes (geniculate, petrosal and nodose) form visceral sensory neurons that innervate taste buds and visceral organs. In the chick embryo, the ophthalmic trigeminal (opV) placode expresses the paired homeodomain transcription factor Pax3 from very early stages, while the epibranchial Placodes express Pax2. Here, we show that Pax3 expression in explanted opV placode ectoderm correlates at the single cell level with neuronal specification and with commitment to an opV fate. When opV (trigeminal) ectoderm is grafted in place of the nodose (epibranchial) placode, Pax3-expressing cells form Pax3-positive neurons on the same schedule as in the opV placode. In contrast, Pax3-negative cells in the grafted ectoderm are induced to express the epibranchial placode marker Pax2 and form neurons in the nodose ganglion that express the epibranchial neuron marker Phox2a on the same schedule as host nodose neurons. They also project neurites along central and peripheral nodose neurite pathways and survive until well after the main period of cell death in the nodose ganglion. The older the opV ectoderm is at the time of grafting, the more Pax3-positive cells it contains and the more committed it is to an opV fate. Our results suggest that, within the Neurogenic Placodes, there does not appear to be a two-step induction of 'generic' neurons followed by specification of the neuron to a particular fate. Instead, there seems to be a one-step induction in which neuronal subtype identity is coupled to neuronal differentiation.

Susanne Dietrich - One of the best experts on this subject based on the ideXlab platform.

Anthony Graham - One of the best experts on this subject based on the ideXlab platform.

  • Neural tube derived Wnt signals cooperate with FGF signaling in the formation and differentiation of the trigeminal Placodes
    Neural Development, 2008
    Co-Authors: Claire A Canning, Anthony Graham, Lily Lee, Sarah Xinwei Luo, C Michael Jones
    Abstract:

    Background Neurogenic Placodes are focal thickenings of the embryonic ectoderm that form in the vertebrate head. It is within these structures that the precursors of the majority of the sensory neurons of the cranial ganglia are specified. The trigeminal Placodes, the ophthalmic and maxillomandibular, form close to the midbrain-hindbrain boundary and many lines of evidence have shown that signals emanating from this level of the neuraxis are important for the development of the ophthalmic placode. Results Here, we provide the first evidence that both the ophthalmic and maxillomandibular Placodes form under the influence of isthmic Wnt and FGF signals. Activated Wnt signals direct development of the Pax3 expressing ophthalmic placodal field and induce premature differentiation of both the ophthalmic and the maxillomandibular Placodes. Similarly, overexpression of Fgf8 directs premature differentiation of the trigeminal Placodes. Wnt signals require FGF receptor activity to initiate Pax3 expression and, subsequently, the expression of neural markers, such as Brn3a , within the cranial ectoderm. Furthermore, fibroblast growth factor signaling via the mitogen activated protein kinase pathway is required to maintain early neuronal differentiation within the trigeminal Placodes. Conclusion We demonstrate the identity of inductive signals that are necessary for trigeminal ganglion formation. This is the first report that describes how isthmic derived Wnt signals act in concert with fibroblast growth factor signaling. Together, both are necessary and sufficient for the establishment and differentiation of the ophthalmic and maxillomandibular Placodes and, consequently, the trigeminal ganglion.

  • delamination of cells from Neurogenic Placodes does not involve an epithelial to mesenchymal transition
    Development, 2007
    Co-Authors: Anthony Graham, Aida Blentic, Sandra Duque, Jo Begbie
    Abstract:

    Neurogenic Placodes are specialized regions of embryonic ectoderm that generate the majority of the neurons of the cranial sensory ganglia. Here we examine in chick the mechanism underlying the delamination of cells from the epibranchial placodal ectoderm. We show that the placodal epithelium has a distinctive morphology, reflecting a change in cell shape, and is associated with a breach in the underlying basal lamina. Placodal cell delamination is distinct from neural crest cell delamination. In particular, exit of neuroblasts from the epithelium is not associated with the expression of Snail/Snail2 or of the Rho family GTPases required for the epithelial-to-mesenchymal transition seen in neural crest cell delamination. Indeed, cells leaving the Placodes do not assume a mesenchymal morphology but migrate from the epithelium as neuronal cells. We further show that the placodal epithelium has a pseudostratified appearance. Examination of proliferation shows that the placodal epithelium is mitotically quiescent, with few phosphohistone H3-positive cells being identified. Where division does occur within the epithelium it is restricted to the apical surface. The Neurogenic Placodes thus represent specialized ectodermal niches that generate neuroblasts over a protracted period.

  • Early steps in the production of sensory neurons by the Neurogenic Placodes.
    Molecular and cellular neurosciences, 2002
    Co-Authors: Joanne Begbie, Marc Ballivet, Anthony Graham
    Abstract:

    Abstract NeurogenicPlacodes are specialized regions of the embryonic ectoderm that generate the majority of the neurons of the cranial sensory ganglia. Here we have accurately determined the onset of neurogenesis in each of the Placodes in the chick, and we have also analyzed the expression profiles of genes that are believed to be involved in determining the types of sensory neurons produced by each placode. Interestingly, we find that there is a major difference in the expression domains of neurogenin-1 and neurogenin-2 in the chick, when compared with those reported for the mouse. We do find, however, that Brn-3a and Phox-2a and Phox-2b which are also associated with the specification of neuronal type are expressed in the same domains in the chick as they are in the mouse. These results suggest that neurogenin-1 and neurogenin-2 are functionally interchangeable in Neurogenic Placodes. We have also found major differences between the ophthalmic and maxillomandibular trigeminal Placodes, and while all of the other Placodes generate mitotically active cells the ophthalmic trigeminal placode seems to throw off postmitotic neuronal cells.

  • Neurogenic Placodes: a common front
    Trends in neurosciences, 2000
    Co-Authors: Anthony Graham, Jo Begbie
    Abstract:

    Abstract Neurogenic Placodes are specialized regions of the embryonic ectoderm that are central to the development of the cranial sensory systems of vertebrates. These structures generate many of the sensory neurones of the head and also, in some instances, the associated sensory receptor cells. The Neurogenic Placodes have often been thought to share common pathways of development and to have evolved together. However, recent work has shown that this is not the case. The term ‘Neurogenic Placodes' no longer seems to describe a cohesive group. Rather, the Neurogenic Placodes fall into a number of categories, and it is within each of these that the members share a common development and evolution.

Gerhard Schlosser - One of the best experts on this subject based on the ideXlab platform.

  • Eya1 and Six1 promote neurogenesis in the cranial Placodes in a SoxB1-dependent fashion
    Developmental Biology, 2008
    Co-Authors: Gerhard Schlosser, Tammy Awtry, Samantha A. Brugmann, Eric D. Jensen, Karen M. Neilson, Gui Ruan, Angelika Stammler, Doris Voelker, Bo Yan, Chi Zhang
    Abstract:

    Genes of the Eya family and of the Six1/2 subfamily are expressed throughout development of vertebrate cranial Placodes and are required for their differentiation into ganglia and sense organs. How they regulate placodal neurogenesis, however, remains unclear. Through loss of function studies in Xenopus we show that Eya1 and Six1 are required for neuronal differentiation in all Neurogenic Placodes. The effects of overexpression of Eya1 or Six1 are dose dependent. At higher levels, Eya1 and Six1 expand the expression of SoxB1 genes (Sox2, Sox3), maintain cells in a proliferative state and block expression of neuronal determination and differentiation genes. At lower levels, Eya1 and Six1 promote neuronal differentiation, acting downstream of and/or parallel to Ngnr1. Our findings suggest that Eya1 and Six1 are required for both the regulation of placodal neuronal progenitor proliferation, through their effects on SoxB1 expression, and subsequent neuronal differentiation.

  • Xenopus Eya1 demarcates all Neurogenic Placodes as well as migrating hypaxial muscle precursors
    Mechanisms of Development, 2001
    Co-Authors: Robert David, Katja Ahrens, Doris Wedlich, Gerhard Schlosser
    Abstract:

    We cloned two isoforms of the Xenopus Eya1 orthologue. They show identical patterns of expression that closely resemble the previously described expression of XSix1, but partly differ from the expression of Eya1 in other vertebrates. XEya1 is expressed in the somites and hypaxial muscle precursors, but not in the pronephros. Moreover, all ectodermal Placodes except the lens placode strongly express XEya1. At neural plate stages, ectodermal XEya1 expression starts in two domains, the anterior neural folds and a domain lateral to the neural folds. At tailbud stages, XEya1 expression continues in the adenohypophysis, all Neurogenic Placodes and placodally-derived structures including cranial ganglia, the otic vesicle and lateral line primordia.

  • development of Neurogenic Placodes in xenopus laevis
    The Journal of Comparative Neurology, 2000
    Co-Authors: Gerhard Schlosser, Glenn R Northcutt
    Abstract:

    The development of Neurogenic Placodes in Xenopus laevis from the time of neural fold closure to larval stages is described. Placodes were reconstructed from camera lucida drawings of serial sections, and the spatiotemporal pattern of placodal neurogenesis was analyzed using in situ hybridization for the genes X-NGNR-1, XNeuroD, X-MyT1, and X-Delta-1, all of which have been implicated in the regulation of neurogenesis. Olfactory, profundal, and trigeminal Placodes, a series of dorsolateral Placodes (otic placode and five lateral line Placodes), a series of epibranchial Placodes, and two hypobranchial Placodes were identified. Earlier claims that all Placodes in anurans develop from a common primordium could not be confirmed. Profundal and trigeminal Placodes, however, are partially fused, and all lateral line Placodes arise from a common precursor. Epibranchial and hypobranchial Placodes develop ventral to other Placodes and dorsal and ventral to the pharyngeal pouches, respectively. Hypobranchial Placodes give rise to neurons that become intimately associated with the developing heart. All Neurogenic Placodes strongly express the neuronal differentiation gene XNeuroD. The neuronal determination gene X-NGNR-1, however, is expressed strongly in only some Placodes and not in dorsolateral Placodes, indicating that neurogenesis in the latter relies on other determination genes. X-Delta-1 is expressed not only in the Neurogenic parts of the Placodes but also in the primordia of the lateral lines. This suggests that Delta-Notch-mediated lateral inhibition may be involved not only in placodal neurogenesis, but also in the patterning of lateral line neuromasts. J. Comp. Neurol. 418:121–146, 2000. © 2000 Wiley-Liss, Inc.