Biomedical subjects

J Begbie

Publications and source records attributed to J Begbie.

7 recordsLinked to original sources

PubMed2001

The ectodermal placodes: a dysfunctional family.

The ectodermal placodes are focal thickenings of the cranial embryonic ectoderm that contribute extensively to the cranial sensory systems of the vertebrates. The ectodermal placodes have long been thought of as representing a coherent group, which share a developmental and evolutionary history. However, it is now becoming clear that there are substantial differences between the placodes with respect to their early development, their induction and their evolution. Indeed, it is now hard to consider the ectodermal placodes as a single entity. Rather, they fall into a number of distinct classes and it is within each of these that the members share a common development and evolution.

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PubMed2001

Integration between the epibranchial placodes and the hindbrain.

Developmental integration results from coordination among components of different embryonic fields to realize the later anatomical and functional relationships. We demonstrate that in the chick head, integration between the epibranchial placodes and the hindbrain is achieved as the neuroglial hindbrain crest cells guide the epibranchial neuronal cells inward to establish their central connections. This work defines a role for the neuroglial hindbrain crest in organizing the afferent innervation of the hindbrain.

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PubMed2001

Early development of the mesencephalic trigeminal nucleus.

The cells of the mesencephalic trigeminal nucleus (MTN) are the proprioceptive sensory neurons that innervate the jaw muscles. Interestingly, their evolution is generally thought to have been concomitant with that of the jaws. They are also the first born neurons of the mesencephalon, and their axons pioneer some of the major tracts within the brain. The cells of the MTN are also paradoxical in being the only group of intramedullary primary sensory neurons in amniotes. However, we know little about the early development of these important neurons, and we have analysed this here. To study the earliest stages of MTN development, we have used a battery of neural crest markers to try and pinpoint the progenitors of the MTN. We find that, contrary to current perceptions, the progenitors of the MTN are not highlighted by these markers, suggesting that they are not neural crest derived. However, the cells of the MTN are marked by means of their expression of Brn-3a. This gene labels cells that arise either side of the dorsal midline, extending rostrally from the isthmus across the roof of the mesencephalon. We have further demonstrated that the MTN develops under the influence of the Fgf-8 secreted by the isthmus. Ectopic Fgf-8 application promotes MTN development, whereas inhibiting Fgf-8 function in vivo drastically affects MTN development.

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PubMed2000

Neurogenic placodes: a common front.

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.

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PubMed1999

Induction of the epibranchial placodes.

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.

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PubMed1998

NT-3 regulates expression of Brn3a but not Brn3b in developing mouse trigeminal sensory neurons.

We have used a quantitative RT-PCR approach to determine the levels of Brn3a and Brn3b POU domain transcription factor mRNAs in the developing mouse trigeminal ganglion from E10 to E18. Using low density neuronal cultures, we have shown that NT-3 can regulate the expression of Brn3a mRNA in trigeminal neurons during the periods that they are differentiating and innervating their peripheral and central targets. In contrast to Brn3a, Brn3b mRNA is expressed at extremely low levels in the early trigeminal ganglion. Trigeminal neurons from early ganglia express low levels of Brn3b mRNA in culture and do not up-regulate Brn3b mRNA in response to a number of growth factors and experimental conditions. However, at later ages, when in vivo levels of Brn3b mRNA are high, FGF2, TGFbeta1 and retinoic acid all up-regulate Brn3b mRNA expression in cultured trigeminal neurons. Since NT-3 regulates the developmental expression of Brn3a, Brn3a may mediate some of the effects that NT-3 exerts on sensory neurons and their progenitors. Similarly, Brn3b may mediate some of the effects that FGF2, TGFbeta1 and retinoic acid have on neurons.

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PubMedDate not supplied

Pharyngeal arch patterning in the absence of neural crest.

Pharyngeal arches are a prominent and critical feature of the developing vertebrate head. They constitute a series of bulges within which musculature and skeletal elements form; importantly, these tissues derive from different embryonic cell types [1]. Numerous studies have emphasised the role of the cranial neural crest, from which the skeletal components derive, in patterning the pharyngeal arches [2-4]. It has never been clear, however, whether all arch patterning is completely dependent on this cell type. Here, we show that pharyngeal arch formation is not coupled to the process of crest migration and, furthermore, that pharyngeal arches form, are regionalized and have a sense of identity even in the absence of the neural crest. Thus, vertebrate head morphogenesis can now be seen to be a more complex process than was previously believed and must result from an integration of both neural-crest-dependent and -independent patterning mechanisms. Our results also reflect the fact that the evolutionary origin of pharyngeal segmentation predates that of the neural crest, which is an exclusively vertebrate characteristic.

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