scholarly journals Radial glial progenitors repair the zebrafish spinal cord following transection

2014 ◽  
Vol 256 ◽  
pp. 81-92 ◽  
Author(s):  
Lisa K. Briona ◽  
Richard I. Dorsky
2020 ◽  
Vol 16 (72) ◽  
pp. 229
Author(s):  
V.S. Shkolnikov ◽  
S.O. Prykhodko ◽  
S.S. Polishchuk ◽  
O.V. Kryvoviaz ◽  
G.М. Galunko

Stem Cells ◽  
2009 ◽  
Vol 27 (11) ◽  
pp. 2722-2733 ◽  
Author(s):  
Jean-Charles Sabourin ◽  
Karin B. Ackema ◽  
David Ohayon ◽  
Pierre-Olivier Guichet ◽  
Florence E. Perrin ◽  
...  

2020 ◽  
Author(s):  
Zhongfu Shen ◽  
Yang Lin ◽  
Jiajun Yang ◽  
David J. Jörg ◽  
Yuwei Peng ◽  
...  

SUMMARYRadial glial progenitors (RGPs) are responsible for producing the vast majority of neurons and glia in the neocortex. While RGP behavior and progressive generation of neocortical neurons have been delineated, the exact process of neocortical gliogenesis remains elusive. Here, we report the precise progenitor cell behavior and gliogenesis program at single-cell resolution in the mouse neocortex. RGPs transition from neurogenesis to gliogenesis progressively, producing astrocytes, oligodendrocytes, or both in well-defined propensities of 60%:15%:25%, respectively, via fate-restricted “intermediate” precursor cells. While the total number of precursor cells generated by individual RGPs appears stochastic, the output of individual precursor cells exhibit clear patterns in number and subtype, and form discrete local subclusters. Clonal loss of tumor suppressor Neurofibromatosis type 1 leads to excessive production of glia selectively, especially oligodendrocyte precursor cells. These results delineate the cellular program of neocortical gliogenesis quantitatively and suggest the cellular and lineage origin of primary brain tumor.


2005 ◽  
Vol 15 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Leah Ever ◽  
Nicholas Gaiano

2005 ◽  
Vol 68 (5) ◽  
pp. 361-369 ◽  
Author(s):  
Marjan Moreels ◽  
Frank Vandenabeele ◽  
Leen Deryck ◽  
Ivo Lambrichts

Neuroreport ◽  
2010 ◽  
Vol 21 (13) ◽  
pp. 871-876 ◽  
Author(s):  
Hiroshi Nomura ◽  
Howard Kim ◽  
Andrea Mothe ◽  
Tasneem Zahir ◽  
Iris Kulbatski ◽  
...  

2005 ◽  
Vol 27 (6) ◽  
pp. 364-377 ◽  
Author(s):  
Yasuhiro Ogawa ◽  
Hirohide Takebayashi ◽  
Masanori Takahashi ◽  
Noriko Osumi ◽  
Yasuno Iwasaki ◽  
...  

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.


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