Semaphorin and neuropilin expression during early morphogenesis of <i>Xenopus laevis</i>

Koestner, Ulrich; Shnitsar, Iryna; Linnemannstöns, Karen; Hufton, Andrew L.; Borchers, Annette

doi:10.1002/dvdy.21785

Cited by 29 publications

(29 citation statements)

References 33 publications

(40 reference statements)

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“…Nrp1-semaphorin signaling regulates neural crest migration, which affects placode contributions to cranial ganglia in Xenopus and mouse (Koestner et al, 2008; Schwarz et al 2008). PDGF signaling can induce ophthalmic placode formation (McCabe and Bronner-Fraser, 2008) and in combination with FGF plays a role in PPR specification (Kwon et al, 2010).…”

Section: Resultsmentioning

confidence: 99%

Microarray identification of novel genes downstream of Six1, a critical factor in cranial placode, somite, and kidney development

Yan

Neilson

Ranganathan

et al. 2014

Developmental Dynamics

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Background Six1 plays an important role in the development of several vertebrate organs, including cranial sensory placodes, somites and kidney. Although Six1 mutations cause one form of Branchio-Otic Syndrome (BOS), the responsible gene in many patients has not been identified; genes that act downstream of Six1 are potential BOS candidates. Results We sought to identify novel genes expressed during placode, somite and kidney development by comparing gene expression between control and Six1-expressing ectodermal explants. The expression patterns of 19 of the significantly up-regulated and 11 of the significantly down-regulated genes were assayed from cleavage to larval stages. 28/30 genes are expressed in the otocyst, a structure that is functionally disrupted in BOS, and 26/30 genes are expressed in the nephric mesoderm, a structure that is functionally disrupted in the related Branchio-Otic-Renal (BOR) syndrome. We also identified the chick homologues of 5 genes and show that they have conserved expression patterns. Conclusions Of the 30 genes selected for expression analyses, all are expressed at many of the developmental times and appropriate tissues to be regulated by Six1. Many have the potential to play a role in the disruption of hearing and kidney function seen in BOS/BOR patients.

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Section: Resultsmentioning

confidence: 99%

Microarray identification of novel genes downstream of Six1, a critical factor in cranial placode, somite, and kidney development

Yan

Neilson

Ranganathan

et al. 2014

Developmental Dynamics

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“…Because genetic ablation of NRP2 results in disorganization of segmental migration of NCCs [85], non-segmental arrangement of intramedullary EGFP-positive cells in Six1/4 EGFP/EGFP might be due to the lack of NRP2 expression rather than the physical isolation mentioned above. Interestingly, Nrp1, but not Nrp2, is also expressed inside Xenopus spinal cord [86], where RB cells exist, suggesting that the combined expression of Nrps is a potential molecular basis for the non-segmental arrangement of intramedullary sensory neurons.…”

Section: Discussionmentioning

confidence: 99%

Six1 is a key regulator of the developmental and evolutionary architecture of sensory neurons in craniates

et al. 2014

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BackgroundVarious senses and sensory nerve architectures of animals have evolved during adaptation to exploit diverse environments. In craniates, the trunk sensory system has evolved from simple mechanosensory neurons inside the spinal cord (intramedullary), called Rohon-Beard (RB) cells, to multimodal sensory neurons of dorsal root ganglia (DRG) outside the spinal cord (extramedullary). The fish and amphibian trunk sensory systems switch from RB cells to DRG during development, while amniotes rely exclusively on the DRG system. The mechanisms underlying the ontogenic switching and its link to phylogenetic transition remain unknown.ResultsIn Xenopus, Six1 overexpression promoted precocious apoptosis of RB cells and emergence of extramedullary sensory neurons, whereas Six1 knockdown delayed the reduction in RB cell number. Genetic ablation of Six1 and Six4 in mice led to the appearance of intramedullary sensory neuron-like cells as a result of medial migration of neural crest cells into the spinal cord and production of immature DRG neurons and fused DRG. Restoration of SIX1 expression in the neural crest-linage partially rescued the phenotype, indicating the cell autonomous requirements of SIX1 for normal extramedullary sensory neurogenesis. Mouse Six1 enhancer that mediates the expression in DRG neurons activated transcription in Xenopus RB cells earlier than endogenous six1 expression, suggesting earlier onset of mouse SIX1 expression than Xenopus during sensory development.ConclusionsThe results indicated the critical role of Six1 in transition of RB cells to DRG neurons during Xenopus development and establishment of exclusive DRG system of mice. The study provided evidence that early appearance of SIX1 expression, which correlated with mouse Six1 enhancer, is essential for the formation of DRG-dominant system in mice, suggesting that heterochronic changes in Six1 enhancer sequence play an important role in alteration of trunk sensory architecture and contribute to the evolution of the trunk sensory system.

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“…It is at this point that Xenopus RGCs initiate expression of Nrp1 and Plxna1, equipping their axons with the ability to respond to Sema3a as a repellent both in vitro and in vivo (AtkinsonLeadbeater et al, 2010;Campbell et al, 2001). Intriguingly, a number of Sema3 genes are expressed in the retina after the majority of RGC axons have left the eye and the dendrites start to emerge (Callander et al, 2007;Koestner et al, 2008). As such, we investigated whether Nrp and PlxnA receptors regulate the growth of RGC dendrites in vivo.…”

Section: Introductionmentioning

confidence: 99%

Neuropilin-1 biases dendrite polarization in the retina

et al. 2013

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SUMMARYThe majority of neurons in the nervous system exhibit a polarized morphology, with multiple short dendrites and a single long axon. It is clear that multiple factors govern polarization in developing neurons, and the biased accumulation of intrinsic determinants to one side of the cell, coupled with responses to asymmetrically localized extrinsic factors, appears to be crucial. A number of intrinsic factors have been identified, but surprisingly little is known about the identity of the extrinsic signals. Here, we show in vivo that neuropilin-1 (Nrp1) and its co-receptor plexinA1 (Plxna1) are necessary to bias the extension of the dendrites of retinal ganglion cells to the apical side of the cell, and ectopically expressed class III semaphorins (Sema3s) disrupt this process. Importantly, the requirement for Nrp1 and Plxna1 in dendrite polarization occurs at a developmental time point after the cells have already extended their basally directed axon. Thus, we propose a novel mechanism whereby an extrinsic factor, probably a Sema3, acts through Nrp1 and Plxna1 to promote the asymmetric outgrowth of dendrites independently of axon polarization.

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Semaphorin and neuropilin expression during early morphogenesis of Xenopus laevis

Cited by 29 publications

References 33 publications

Microarray identification of novel genes downstream of Six1, a critical factor in cranial placode, somite, and kidney development

Microarray identification of novel genes downstream of Six1, a critical factor in cranial placode, somite, and kidney development

Six1 is a key regulator of the developmental and evolutionary architecture of sensory neurons in craniates

Neuropilin-1 biases dendrite polarization in the retina

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