scholarly journals Multiple steps mediate ventricular layer attrition to form the adult mouse spinal cord central canal

2019 ◽  
Author(s):  
Marco A. Cañizares ◽  
Aida Rodrigo Albors ◽  
Gail Singer ◽  
Nicolle Suttie ◽  
Metka Gorkic ◽  
...  

AbstractThe ventricular layer of the spinal cord is remodelled during embryonic development and ultimately forms the adult central canal, which retains neural stem cell potential. This anatomical transformation involves the process of dorsal collapse, however, accompanying changes in tissue organization and cell behaviour as well as the origin of cells contributing to the adult central canal are not well understood. Here we describe sequential localised cell rearrangements which contribute to the gradual attrition of the spinal cord ventricular layer during development. This includes local breakdown of the pseudostratified organisation of the dorsal ventricular layer prefiguring dorsal collapse and evidence for a new phenomenon, ventral dissociation, during which the ventral-most floor plate cells separate from a subset that are retained in the central canal. Using cell proliferation markers and cell-cycle reporter mice, we further show that following dorsal collapse, ventricular layer attrition involves an overall reduction in cell proliferation, characterised by an intriguing increase in the percentage of cells in G1/S. In contrast, programmed cell death does not contribute to ventricular layer remodelling. By analysing transcript and protein expression patterns associated with key signalling pathways, we provide evidence for a gradual decline in ventral sonic hedgehog activity and an accompanying ventral expansion of initial dorsal bone morphogenetic protein signalling, which comes to dominate the forming central canal. This study identifies multiple steps that contribute to spinal cord ventricular layer attrition and adds to increasing evidence for the heterogenous origin of the adult spinal cord central canal, which includes cells from the floor plate and the roof plate as well as ventral progenitor domain.

Development ◽  
1993 ◽  
Vol 117 (3) ◽  
pp. 1001-1016 ◽  
Author(s):  
M.D. Goulding ◽  
A. Lumsden ◽  
P. Gruss

Members of the paired box (Pax) gene family are expressed in discrete regions of the developing central nervous system, suggesting a role in neural patterning. In this study, we describe the isolation of the chicken homologues of Pax-3 and Pax-6. Both genes are very highly conserved and share extensive homology with the mouse Pax-3 and Pax-6 genes. Pax-3 is expressed in the primitive streak and in two bands of cells at the lateral extremity of the neural plate. In the spinal cord, Pax-6 is expressed later than Pax-3 with the first detectable expression preceding closure of the neural tube. When the neural tube closes, transcripts of both genes become dorsoventrally restricted in the undifferentiated mitotic neuroepithelium. We show that the removal of the notochord, or implantation of an additional notochord, dramatically alter the dorsoventral (DV) expression patterns of Pax-3 and Pax-6. These manipulations suggest that signals from the notochord and floor plate regulate the establishment of the dorsoventrally restricted expression domains of Pax-3 and Pax-6 in the spinal cord. The rapid changes to Pax gene expression that occur in neural progenitor cells following the grafting of an ectopic notochord suggest that changes to Pax gene expression are an early effect of the notochord on spinal cord patterning.


2019 ◽  
Author(s):  
Christine Tait ◽  
Kavitha Chinnaiya ◽  
Mariyam Murtaza ◽  
John-Paul Ashton ◽  
Nicholas Furley ◽  
...  

AbstractIn the spinal cord, the adult central canal forms through a poorly-understood process termed dorsal collapse that involves attrition and remodelling of the pseudostratified dorsal ventricular layer. Here we show, in mouse, that dorsal ventricular layer cells adjacent to midline Nestin(+) radial glia downregulate the apical polarity proteins Crumbs2 (CRB2) and aPKC and delaminate in a step-wise manner; concomitantly, Nestin(+) radial glial end-feet ratchet down, to repeat this process. Nestin(+) radial glia secrete a factor that promotes cell delamination. This activity is mimicked by a secreted variant of CRB2 (CRB2S), which is specifically expressed by dorsal midline Nestin(+) radial glia. In cultured cells, CRB2S associated with apical membranes and decreased cell cohesion. Analysis of Crb2F/F/Nestin-Cre+/− mice further confirmed an essential role for CRB2 in dorsal collapse. We propose a model in which CRB2S promotes the progressive attrition of the ventricular layer without loss of overall integrity. This novel mechanism may operate more widely to promote orderly progenitor delamination.


Author(s):  
Jill K. Frey ◽  
Aileen Chen ◽  
R. David Heathcote

All cells of the spinal cord originate from the single layer of neuroepithelium that lines the central canal. Since the turn of the century, it has been known that a subclass of these ependymal cells can differentiate into neurons and extend cytoplasmic projections and cilia into the central canal. We have recently used tyrosine hydroxylase immunocytochemistry to identify a catecholaminergic subpopulation of cerebrospinal fluid (CSF) contacting ependymal neurons in the developing spinal cord of the frog Xenopus laevis (Fig. 1). The interneurons are located in the floor plate region of the spinal cord and have axons that extend rostrally toward the hindbrain. During the morphogenesis of the catecholaminergic population of cells, two longitudinal columns gradually appear and then rapidly “converge” at the ventral midline. Transverse sections of embryonic spinal cord (see Fig. 1) showed that the cell bodies decreased in size and underwent changes in shape, number and position within the spinal cord.


Development ◽  
2019 ◽  
Vol 146 (2) ◽  
pp. dev159343 ◽  
Author(s):  
Takuma Shinozuka ◽  
Ritsuko Takada ◽  
Shosei Yoshida ◽  
Shigenobu Yonemura ◽  
Shinji Takada

Stem Cells ◽  
2016 ◽  
Vol 35 (2) ◽  
pp. 485-496 ◽  
Author(s):  
Wenjun Xu ◽  
Nadia Sachewsky ◽  
Ashkan Azimi ◽  
Maurita Hung ◽  
Andrew Gappasov ◽  
...  

2018 ◽  
Vol 368 (1) ◽  
pp. 84-100 ◽  
Author(s):  
Xiaofei Li ◽  
Elisa M. Floriddia ◽  
Konstantinos Toskas ◽  
Chaima Chalfouh ◽  
Axel Honore ◽  
...  

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 411-420 ◽  
Author(s):  
A. Awgulewitsch ◽  
D. Jacobs

Synthetic oligopeptides derived from the predicted Hox 3.1 protein coding sequence were used for the production of antibodies (anti-aa2) that specifically recognize Hox 3.1 protein in tissue sections. These antibodies were applied in immunohistochemical studies to monitor the expression of Hox 3.1 protein within the central nervous system (CNS) of embryonic and adult mice. We demonstrate congruency between the distinct Hox 3.1 RNA and protein expression patterns in the developing spinal cord by direct comparison of in situ hybridization and immunohistochemical staining in frozen sagittal sections from embryos of 12.5 days of gestation. A distinct pattern of spatially restricted expression of Hox 3.1 protein within the spinal cord was first detected at around 10.5 days of embryonic development. Within certain anteroposterior limits the geometries of this expression pattern change drastically during subsequent embryonic stages, concomitant with important cytoarchitectural changes in the developing spinal cord. Analyses on subcellular levels indicate predominant accumulation of Hox 3.1 protein within nuclei of neuronal cells. In addition to the nuclear localization in subsets of embryonic cells, persistent accumulation of Hox 3.1 protein was shown in nuclei of fully differentiated and mature neuronal cells of the adult CNS.


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