Expression analysis of chick Frizzled receptors during spinal cord development

FZD10 regulates cell proliferation and mediates Wnt1 induced neurogenesis in the developing spinal cord

10.1101/690263 ◽

2019 ◽

Author(s):

Abdulmajeed Fahad Alrefaei ◽

Andrea E. Münsterberg ◽

Grant N. Wheeler

Keyword(s):

Spinal Cord ◽

Cell Proliferation ◽

Neural Tube ◽

Spinal Cord Development ◽

Dorsal Neural Tube ◽

Wnt Ligands ◽

Frizzled Receptors ◽

Developmental Contexts ◽

Developing Spinal Cord

AbstractWnt/FZD signalling activity is required for spinal cord development, including the dorsal-ventral patterning of the neural tube, where it affects proliferation and specification of neurons. Wnt ligands initiate canonical, β-catenin-dependent, signaling by binding to Frizzled receptors. However, in many developmental contexts the cognate FZD receptor for a particular Wnt ligand remains to be identified. Here, we characterized FZD10 expression in the dorsal neural tube where it overlaps with both Wnt1 and Wnt3a, as well as markers of dorsal progenitors and interneurons. We show FZD10 expression is sensitive to Wnt1, but not Wnt3a expression, and FZD10 plays a role in neural tube patterning. Knockdown approaches show that Wnt1 induced ventral expansion of dorsal neural markes, Pax6 and Pax7, requires FZD10. In contrast, Wnt3a induced dorsalization of the neural tube is not affected by FZD10 knockdown. Gain of function experiments show that FZD10 is not sufficient on its own to mediate Wnt1 activity in vivo. Indeed excess FZD10 inhibits the dorsalizing activity of Wnt1. However, addition of the Lrp6 co-receptor dramatically enhances the Wnt1/FZD10 mediated activation of dorsal markers. This suggests that the mechanism by which Wnt1 regulates proliferation and patterning in the neural tube requires both FZD10 and Lrp6.

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An Early Developmental Marker for Radial Glia in Rat Spinal Cord

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100162648 ◽

1996 ◽

Vol 54 ◽

pp. 36-37

Author(s):

V. Kriho ◽

H.-Y. Yang ◽

C.-M. Lue ◽

N. Lieska ◽

G. D. Pappas

Keyword(s):

Spinal Cord ◽

Intermediate Filament ◽

Radial Glia ◽

Rat Spinal Cord ◽

Future Studies ◽

Spinal Cord Development ◽

Median Septum ◽

Differentiation Marker ◽

Early Developmental ◽

Developing Rat

Radial glia have been classically defined as those early glial cells that radially span their thin processes from the ventricular to the pial surfaces in the developing central nervous system. These radial glia constitute a transient cell population, disappearing, for the most part, by the end of the period of neuronal migration. Traditionally, it has been difficult to definitively identify these cells because the principal criteria available were morphologic only.Using immunofluorescence microscopy, we have previously defined a phenotype for radial glia in rat spinal cord based upon the sequential expression of vimentin, glial fibrillary acidic protein and an intermediate filament-associated protein, IFAP-70/280kD. We report here the application of another intermediate filament-associated protein, IFAP-300kD, originally identified in BHK-21 cells, to the immunofluorescence study of radial glia in the developing rat spinal cord.Results showed that IFAP-300kD appeared very early in rat spinal cord development. In fact by embryonic day 13, IFAP-300kD immunoreactivity was already at its peak and was observed in most of the radial glia which span the spinal cord from the ventricular to the subpial surfaces (Fig. 1). Interestingly, from this time, IFAP-300kD immunoreactivity diminished rapidly in a dorsal to ventral manner, so that by embryonic day 16 it was detectable only in the maturing macroglial cells in the marginal zone of the spinal cord and the dorsal median septum (Fig. 2). By birth, the spinal cord was essentially immuno-negative for this IFAP. Thus, IFAP-300kD appears to be another differentiation marker available for future studies of gliogenesis, especially for the early stages of radial glia differentiation.

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Glycine Release from Radial Cells Modulates the Spontaneous Activity and Its Propagation during Early Spinal Cord Development

Journal of Neuroscience ◽

10.1523/jneurosci.2115-09.2010 ◽

2010 ◽

Vol 30 (1) ◽

pp. 390-403 ◽

Cited By ~ 46

Author(s):

A.-L. Scain ◽

H. Le Corronc ◽

A.-E. Allain ◽

E. Muller ◽

J.-M. Rigo ◽

...

Keyword(s):

Spinal Cord ◽

Spontaneous Activity ◽

Spinal Cord Development ◽

Glycine Release

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Diminished ventral oligodendrocyte precursor generation results in the subsequent over-production of dorsal oligodendrocyte precursors of aberrant morphology and function

10.1101/2020.03.09.983908 ◽

2020 ◽

Author(s):

Lev Starikov ◽

Andreas H. Kottmann

Keyword(s):

Spinal Cord ◽

Motor Neurons ◽

Ventricular Zone ◽

Normal Numbers ◽

Spinal Cord Development ◽

Oligodendrocyte Precursor ◽

And Function ◽

Sod1 Mouse ◽

Lateral Sclerosis ◽

Ventral Spinal Cord

AbstractOligodendrocyte precursor cells (OPCs) arise sequentially first from a ventral and then from a dorsal precursor domain at the end of neurogenesis during spinal cord development. Whether the sequential production of OPCs is of physiological significance has not been examined. Here we show that ablating Shh signaling from nascent ventricular zone derivatives and partially from the floor plate results in a severe diminishment of ventral derived OPCs but normal numbers of motor neurons in the postnatal spinal cord. In the absence of ventral vOPCs, dorsal dOPCs populate the entire spinal cord resulting in an increased OPC density in the ventral horns. These OPCs take on an altered morphology, do not participate in the removal of excitatory vGlut1 synapses from injured motor neurons, and exhibit morphological features similar to those found in the vicinity of motor neurons in the SOD1 mouse model of Amyotrophic Lateral Sclerosis (ALS). Our data indicates that vOPCs prevent dOPCs from invading ventral spinal cord laminae and suggests that vOPCs have a unique ability to communicate with injured motor neurons.

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Primary Cilia, Sonic Hedgehog Signaling, and Spinal Cord Development

Cilia and Nervous System Development and Function ◽

10.1007/978-94-007-5808-7_2 ◽

2012 ◽

pp. 55-82 ◽

Cited By ~ 4

Author(s):

Laura E. Mariani ◽

Tamara Caspary

Keyword(s):

Spinal Cord ◽

Sonic Hedgehog ◽

Hedgehog Signaling ◽

Primary Cilia ◽

Sonic Hedgehog Signaling ◽

Spinal Cord Development

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2 Normal Spinal Cord Development and the Embryogenesis of Spinal Cord Tethering Malformations

Tethered Cord Syndrome in Children and Adults ◽

10.1055/b-0034-80500 ◽

2010 ◽

Keyword(s):

Spinal Cord ◽

Spinal Cord Development ◽

Spinal Cord Tethering

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Spinal development and spinal dysraphism

Oxford Textbook of Neurological Surgery ◽

10.1093/med/9780198746706.003.0085 ◽

2019 ◽

pp. 983-992

Author(s):

Dominic Thompson

Keyword(s):

Spinal Cord ◽

Spinal Dysraphism ◽

Radical Resection ◽

Management Plan ◽

Congenital Disorders ◽

Spinal Cord Development ◽

Precise Diagnosis ◽

Over Time ◽

Spinal Cord Tethering

The term spinal dysraphism encompasses a group of congenital disorders of spinal cord development. This potentially confusing array of conditions is best understood from an embryological perspective, and a unifying method of classification is presented. Spinal dysraphism is associated with neurological, urological, and orthopaedic deficits, these may be present at birth or may evolve over time due to the effects of spinal cord tethering. Precise diagnosis is essential to formulating an appropriate surgical management plan in order to optimize long-term neurological outcome. Contemporary and controversial surgical advances in the field are discussed including electrophysiology directed radical resection for spinal lipomas and antenatal surgery for myelomeningocele.

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