Edwards-Faret G , González-Pinto K , Cebrián-Silla A , Peñailillo J , García-Verdugo JM , Larraín J .

PFB 12/2007 CARE Chile UC-Centro de Envejecimiento y Regeneración, RC120003 MINREB, 1141162 FONDECYT, PROMETEOII/2014/075 Prometeo grant, 21110043 Gastos Operacionales-CONICYT, Chile-2016 FWIS L'Oreal-Unesco

Xla.Tg(Dre.gfap:mCherry-NTR) + MTZ (Fig. 7. H (green))
Xla.Tg(Dre.gfap:mCherry-NTR) + MTZ (Fig. 7 K L)
Xla Wt + spinal cord amputation (Fig. 2. C-M)
Xla Wt + spinal cord amputation (Fig. 6 C-M)

	Fig. 1. Cellular response to injury in Regenerative Stage. a Cartoon of spinal cord injury in NF stage 50. b, c Semithin sections of the b rostral and c caudal stumps at 2 days post transection (dpt) stained with methylene blue. Arrowheads in panel C showed macrophages. d-i; k-m; o-s; u, v Correspond to ultrathin sections observed by transmission electron microscopy. d-i Different regions of the spinal cord at 2 dpt; d cells lining the central canal (cc) closing the rostral stump (black arrowhead); e mitochondrial swelling (black arrow) observed in cells from panel D; black arrowheads depict the separation between two cells; f, g mitotic clusters of cells (yellow shadow); h cell undergoing extrusion (purple shadow); i macrophage from panel C from the injured site. j Semithin section at 6 dpt. k-m Different regions of the spinal cord at 6 dpt; k cells in the central canal of the caudal stump (green shadow), without contact with ependymal cells (black arrowheads); l synaptic density (black arrowheads) and synaptic vesicles (white arrowheads); m cells forming a rosette structure in the ablation gap (red shadow). n Semithin section at 10 dpt. o-s Different regions of the spinal cord at 10 dpt; o a bundle of unmyelinated axons surrounded by ependymal cells (black arrowheads); p unmyelinated axon (orange shadow), and synaptic vesicles (white arrowheads); q desmosome junction (black arrowhead) between ependymal cells next to unmyelinated axons; r a myelinated axon (white arrowhead) in the cc of the caudal stump; s neuronal nuclei in the cc of the caudal stump (black arrowhead). t Semithin section at 20 dpt. u-w Different regions of the spinal cord at 20 dpt; u cells in the cc (red line); v ependymal cells with regular shape in the regenerated spinal cord with apical mitochondria (m); w desmosome junctions between the regenerated ependymal cells (black arrowheads). The red dotted lines indicate the injured site (a, b, c, j, n, t)
	Fig. 2. Cellular response to injury in Non-Regenerative Stage. a Cartoon depicting the process of spinal cord injury in NF stage 66. b Semithin section at 2 dpt. c, d; f-g; i-l; n-p Correspond to ultrathin sections observed by transmission electron microscopy. c, d Different regions of the spinal cord at 2 dpt; c central canal (cc) next to the injured site (black arrowheads); d extracellular matrix and red blood cells (red shadow) in the injury site. e Semithin section at 6 dpt. f, g Different regions of the spinal cord at 6 dpt; f ependymal cells in the rostral stump (black arrowheads); g macrophage (blue line) engulfing red blood cells (red shadow) in the cc. h Semithin section of the caudal stump at 10 dpt. i-l Different regions of the spinal cord at 10 dpt; i ependymal cells near to the injured site; j mitochondria (white arrowhead) in the apical surface of ependymal cell (blue line) in contact with the cc; k glial cell processes next to the injured site (white arrowheads); l intermediate filaments (white arrowheads) in the glial process (green line). m Semithin section at 20 dpt. n-p Different regions of the spinal cord at 20 dpt; n ablation gap (red lines) filled with fibroblast-like cell (white arrowhead), and surrounded by extracellular matrix; o microglial-like cell (cyan line) with abundant rough endoplasmic reticulum (white arrowheads); p abundant Collagen (col) fibers (dots) in the injured site. The red dotted lines indicate the injured site (a, b, e, h, m)
	Fig. 3. Glial cell and extracellular matrix response to spinal cord injury in R-Stage and NR-Stage. a-c Immunostaining against vimentin in a uninjured, and at b 2 and c 6 dpt from animals at NF stage 50. d Western blot against Vimentin (Vim) and GAPDH of spinal cords samples obtained from uninjured (ui), and at 2, 6, 10 and 20 dpt in animals at NF stage 50. e-g Immunostaining against Vimentin in uninjured (e-e’), and at (f, f’) 10 and (g-g’) 20 dpt from animals at NF stage 66. h Western blot against Vim and GAPDH of spinal cords samples obtained from uninjured (ui), and at 2, 6, 10 and 20 dpt in animals at NF stage 66. i-o Immunofluorescence against fibronectin in i uninjured, j 6 dpt, and k 10 dpt in NF stage 50; and l uninjured, m 10 dpt, and n 30 dpt in animals at NF stage 66. o-p Immunofluorescence against CSPG in o uninjured, and p-p’ at 40 dpt in NF stage 66. q-v AFOG staining shown Collagen (blue), cells (orange) and Fibrin (red) in q uninjured, and at r 6 and s 10 dpt in animals at NF stage 50, and in t-t’ uninjured, and at u-u’ 10 and v-v’ 20 dpt from animals at NF stage 66. w Analysis of gene expression change upon spinal cord injury comparing injured animals (Ts) with control sham (sham) surgery at 1, 2 and 6 days after injury in NF stage 50 (1R, 2R and 6R), and NF stage 66 (1NR, 2 NR and 6 NR). Colored and crosses scale indicates the level of increase upon injury in green (+, ++, +++) and decrease in red (−, −−, −−−), data obtained from a previous RNAseq analysis [49]. The red dotted lines (b, f, g, j, m, n, p, r, u, v) and yellow arrows (c, k, s) indicate the injured site. Nuclei stained with Hoechst in blue (a-c; e-g; i-p)
	Fig. 4. Zebrafish regulatory regions of GFAP drive expression of EGFP in neural stem and progenitor cells, and astrocytes in Xenopus laevis spinal cord. A-C Lateral view of EGFP expression in the central nervous system at A, B NF-Stage 43, and C NF-Stage 50. A EGFP expression in the eye, brain and spinal cord (arrowheads). B EGFP/brightfield merge. C Dorsal view of EGFP expression in the optic tectum, hindbrain and spinal cord at NF stage 50. D-F Double staining against D EGFP and E Sox2. Panels F showed merge image, and F’, F” magnifications of the dorsal and ventral cells surrounding the central canal. G-O’ Characterization of EGFP cells by double staining at NF stage 66. G-I” EGFP and Sox2; J-L’ EGFP and Brain lipid-binding protein (BLBP); and M-O’ EGFP and Glutamine synthase (GS). Nuclei are label in blue with Hoechst. P-Q Immunogold staining against EGFP at NF stage 50. P EGFP+ cell in contact with the central canal. P’ Magnification of square in P. Expression of EGFP is visualized by the black dots of the gold staining. P” Magnification of square in P’. Gold staining (black arrowhead) in close apposition with filaments (white arrowhead). Q Endfeet from an EGFP+ cell (colored green) in close contact with blood vessel (colored red). R Gene ontology analysis of the RNAseq from EGFP+ cells revealed the stem cell/neural precursor cell identity of these cells. S Dendrogram of EGFP+ cells and EGFP− cells showing the hierarchical clustering of EGFP+ cells with astrocytes and EGFP− cells with neurons and oligodendrocytes. Scale bar: C, F’-F″: 20 μm; A-B, D-F, I’-I″, L’, O’: 50 μm; G-I, J-L, M-O: 200 μm
	Fig. 5. Response to injury of Neural Stem and Progenitor Cells. a Scheme of EdU treatment. b Click-iT staining for EdU (red), and immunofluorescence against EGFP (green), merge with nuclei (blue) in sham control animals at 2 days post sham operation (dps), and 2 dpt. c Graph of EdU-EGFP positive cells per mm3 at 2 dps (red bar) and 2 dpt (green bar). t-Test, ***: p < 0.001. d, e, f, g, h, i Immunofluorescence against EGFP (green) at NF stage 50 in d uninjured, e 2 days post resection (dpr), f 6 dpr, g 7 dpr, h 10 dpr, and i 20 dpr. Magnifications are shown in panels d’-d”, e’-e”, f’-f”, g’, h’ and i’-i”. j, k, l, m, n, o. Serial sections from the same preparation shown in panels d, e, f, g, h, i double stained for EGFP (green) with the neuronal marker Acetylated tubulin (red), and merge (orange). Nuclei are label in blue with Hoechst. White arrowhead highlights colocalization. Scale bar: d, e, f, g, h, i: 200 μm; d’-d”, e’-e”, f’-f”, g’, h’, i’-i”, j-j”, k-k”, l-l”, m-m”, n-n”, o-o”: 50 μm
	Fig. 6. Analysis of the differentiation of Neural Stem Progenitor Cells in response to spinal cord injury. a Diagram of the experimental procedure. b-m Graphs of the ratio in the mRNA levels for the indicated genes between the EGFP+ cells and EGFP− cells in uninjured (ui), 2 and 6 dpt. b EGFP, c, d NSPCs markers: c sox2, d nestin. e-i neuronal precursor/neurogenic differentiation markers: e achaete-scute homolog 1 (ascl1), f neurogenin2a (neurog2a), g neurogenin3 (neurog3), h neurod1, i doublecortin (dcx). j, k Astrocytes markers: j vimentin-a (vim-a), k aldh1l1. l, m Oligodendrocytes markers: l sox10, m myelin basic protein (mbp). n = 2–3 samples. Standard error bar is included in each graph.
	Fig. 7. Ablation of NSPCs blocks spinal cord regeneration. a Diagram of the treatment of zGFAP::mCherry-NTR transgenic animals with metronidazol (MTZ) or vehicle, followed by spinal cord resection, swimming recording, and histological analysis. b-e Eye imaging (b, d) before treatment, and 7 days after incubation with c vehicle or e MTZ. f, g Spinal cord sections showing mCherry expression f before, and g 7 days after MTZ treatment. h Graph of swimming at 1, 10, 15, 25 dpr in sham (Sh) operated animals treated with MTZ (Sh-MTZ, blue boxes), and resected (Rs) animals incubated with vehicle (Rs-Vehicle, red boxes) or MTZ (Rs-MTZ, green boxes). i-l Immunofluorescence against Sox2 (green) and nuclei stained with Hoechst of spinal cord sections obtained from animals at 30 dpr from the i, j Rs-vehicle, and k, l Rs-MTZ treated groups. Statistics in graph H: ANOVA-one way with Bonferroni post-test, ** p < 0.01, n = 4 independent biological replicates
	Figure S1. Cellular response to spinal cord injury in R- and NR-stages. (A) Centriolar satellite ultrastructure (arrowheads) in cells surrounding the rostral stump. (B) Radial projection of cells lining the central canal (yellow shadow). (C) Neutrophil in the injury site at 2 dpt in animals at NF stage 50. (C-E) Cells lining a rosette structure at 6 dpt are characterized by a (D) basal collagen lamina (blue shadow), (E) interdigitations and adherent junctions (arrowheads), and (F) intermediate filaments (arrowheads). Graphs of the number of red blood cells/μm2 × 105 at (G) 2 and 6 dpt in NF stage 50, and (H) at 2 and 6 dpt in NF stage 66. Graphs of the number of macrophages/μm2 × 105 at (I) 2 and 6 dpt in NF stage 50, and (J) at 2 and 6 dpt in NF stage 66. t-Test: ** p < 0,01; *** p < 0,001; **** p < 0,0001.
	Figure S2. In vivo time-lapse imaging of cells being extruded into the central canal. (A) Rostral stump of the transected spinal cord from a zGFAP::EGFP transgenic animal at R-stage 2 dpt. A time-lapses during 7 h for EGFP and transmitted light (T-PMT) z-stack were capture at the following time points: (B-B′) 0 min; 60 min (C-C′); 120 min (D-D′); 180 min (E-E’); 240 min (F-F′); 300 min (G-G’); 360 min (H-H′). White and purple arrows point to extrusion events from the cells lining the central canal.
	Figure S3. Quantification of Vimentin Western Blot and Collagen AFOG staining. Western blot replicates for Vimentin and GAPDH in uninjured animals (ui), and after 2, 6, 10, 20 dpt in (A, B) R-Stage and (C, D) NR-Stage. Graphs of the adjusted relative density bands of Vimentin to the GAPDH control and normalized to the uninjured sample (ui) in (E) R-stage and (F) NR-stage at 2, 6, 10 and 20 days post transection (dpt) spinal cord samples. (G) Graph of the adjusted collagen staining area relative to the uninjured (ui) animals at 6, 10 dpt of R-stage and 10, 20 dpt of NR-stage. Red line defined no changes of Vimentin levels or Collagen staining. t-Test: * p < 0,05; ** p < 0,01; *** p < 0,001.
	Figure S4. Transgenic line Xla.Tg(Dre.gfap:EGFP)Larra. (A-C) Three different animals’ electroporated in the spinal cord with the CAG promoter driving the expression of EGFP in central canal cells. (D-F) Three different animals electroporated in the spinal cord with the zGFAP::EGFP construct driving specific expression in radial glial like cells in contact with the central canal. (G-J) Animals at different developmental stages of the transgenic line Xla.Tg(Dre.gfap:EGFP)Larra show in expression of EGFP in the neural tubeg at (G-G’) NF stage 23; (H-H′) NF stage 27; (I-I′) NF stage 31 and in the CNS at (J-J’) NF stage 41. (K-M) Double staining against (K) EGFP and (L) Sox2 in coronal section of the spinal cord at NF stage 43. Panels (M) showed merge image, and panels (M’, M”) are magnifications of the dorsal and ventral cells surrounding the central canal.
	Figure S5. RNAseq of EGFP+ and EGFP− cells isolated from the transgenic line Xla.Tg(Dre.gfap:EGFP)Larra. (A) Flow chart of RNAseq bioinformatics analysis from EGFP+ and EGFP− cells. (B) Graph of the Log2 fold change of the differential gene expression between EGFP+ cells versus EGFP− cells after FACS and RNAseq. EGFP expression in EGFP+ cells (green) is highlighted.
	Figure S6. Analysis of EdU+ cells in the intestine. (A-B) Click-iT staining of EdU+ (red) of the intestine in (A) sham control animals (2 dps), and at (B) 2 dpt. Nuclei were stained with Hoechst (blue). (C) Graph of EdU+ cells per mm3 in the intestine. n = 3.
	Figure S7. Transgenic line Xla.Tg(Dre.gfap:mCherry-Nitroreductase) allows selective cell ablation. (A) Diagram of injection and electroporation of the spinal cord at NF stage 50, indicating volume, concentration and parameters of electroporation. (B) Scheme of electroporation of the Dre.gfap:mCherry-Nitroreductase construct and treatment with vehicle or metronidazol (MTZ) at NF stage 50. (C-R) mCherry (red) expression in the spinal cord of animal electroporated at (C-D; I-J) 2 days post electroporation (dpe), before treatment; (E-F; K-L) 4 dpe and 2 days post treatment (dtt); (G-H; M-N) 7 dpe and 5 dtt, and (O- R) at 8 dpe and 6 dtt co-stained with Hoechst (blue). (S) The construct used to generate the transgenic line Xla.Tg(Dre.gfap:mCherry-Nitroreductase). (T, U) mCherry expression in the eye (arrow) and the brain of the transgenic animal at NF stage 42.
	Supplementary Table 1. List of genes, ID number and their respective primer-Forward and primer-Reverse used for RT-qPCR analysis.

Adams, Light-activation of the Archaerhodopsin H(+)-pump reverses age-dependent loss of vertebrate regeneration: sparking system-level controls in vivo. 2013, Pubmed, Xenbase

Adams, Light-activation of the Archaerhodopsin H(+)-pump reverses age-dependent loss of vertebrate regeneration: sparking system-level controls in vivo. 2013, Pubmed , Xenbase
Adusumilli, ROS Dynamics Delineate Functional States of Hippocampal Neural Stem Cells and Link to Their Activity-Dependent Exit from Quiescence. 2021, Pubmed
Alfaro-Cervello, Biciliated ependymal cell proliferation contributes to spinal cord growth. 2012, Pubmed
Al Haj Baddar, Amputation-induced reactive oxygen species signaling is required for axolotl tail regeneration. 2019, Pubmed
Anders, Differential expression analysis for sequence count data. 2010, Pubmed
Anderson, Astrocyte scar formation aids central nervous system axon regeneration. 2016, Pubmed
Anderson, Required growth facilitators propel axon regeneration across complete spinal cord injury. 2018, Pubmed
Baker, All in the family: proneural bHLH genes and neuronal diversity. 2018, Pubmed
Barnabé-Heider, Origin of new glial cells in intact and injured adult spinal cord. 2010, Pubmed
Beattie, Metamorphosis alters the response to spinal cord transection in Xenopus laevis frogs. 1990, Pubmed , Xenbase
Becker, The spinal ependymal zone as a source of endogenous repair cells across vertebrates. 2018, Pubmed
Becker, Neuronal regeneration from ependymo-radial glial cells: cook, little pot, cook! 2015, Pubmed
Bernardos, GFAP transgenic zebrafish. 2006, Pubmed
Bigarella, Stem cells and the impact of ROS signaling. 2014, Pubmed
Briona, Radial glial progenitors repair the zebrafish spinal cord following transection. 2014, Pubmed
Briona, Wnt/ß-catenin signaling is required for radial glial neurogenesis following spinal cord injury. 2015, Pubmed
Cardozo, Reduce, reuse, recycle - Developmental signals in spinal cord regeneration. 2017, Pubmed
Choi, Cone degeneration following rod ablation in a reversible model of retinal degeneration. 2011, Pubmed , Xenbase
Chui, Oxidative stress regulates progenitor behavior and cortical neurogenesis. 2020, Pubmed
Curado, Nitroreductase-mediated cell/tissue ablation in zebrafish: a spatially and temporally controlled ablation method with applications in developmental and regeneration studies. 2008, Pubmed
Diaz Quiroz, Spinal cord regeneration: where fish, frogs and salamanders lead the way, can we follow? 2013, Pubmed
Edwards-Faret, Cellular composition and organization of the spinal cord central canal during metamorphosis of the frog Xenopus laevis. 2018, Pubmed , Xenbase
Edwards-Faret, Spinal cord regeneration in Xenopus laevis. 2017, Pubmed , Xenbase
Fawcett, The glial response to injury and its role in the inhibition of CNS repair. 2006, Pubmed
Fei, CRISPR-mediated genomic deletion of Sox2 in the axolotl shows a requirement in spinal cord neural stem cell amplification during tail regeneration. 2014, Pubmed
Ferreira, Early redox activities modulate Xenopus tail regeneration. 2018, Pubmed , Xenbase
Fiorelli, The adult spinal cord harbors a population of GFAP-positive progenitors with limited self-renewal potential. 2013, Pubmed
Fukazawa, Suppression of the immune response potentiates tadpole tail regeneration during the refractory period. 2009, Pubmed , Xenbase
Gaete, Spinal cord regeneration in Xenopus tadpoles proceeds through activation of Sox2-positive cells. 2012, Pubmed , Xenbase
Gibbs, Metamorphosis and the regenerative capacity of spinal cord axons in Xenopus laevis. 2011, Pubmed , Xenbase
Godwin, Macrophages are required for adult salamander limb regeneration. 2013, Pubmed
Goldshmit, Fgf-dependent glial cell bridges facilitate spinal cord regeneration in zebrafish. 2012, Pubmed
Goldshmit, Different Fgfs have distinct roles in regulating neurogenesis after spinal cord injury in zebrafish. 2018, Pubmed
Göritz, A pericyte origin of spinal cord scar tissue. 2011, Pubmed
Gurtner, Wound repair and regeneration. 2008, Pubmed
Hamilton, Cellular organization of the central canal ependymal zone, a niche of latent neural stem cells in the adult mammalian spinal cord. 2009, Pubmed
Homem, Drosophila neuroblasts: a model for stem cell biology. 2012, Pubmed
Hui, Characterization of Proliferating Neural Progenitors after Spinal Cord Injury in Adult Zebrafish. 2015, Pubmed
Ishibashi, A method for generating transgenic frog embryos. 2008, Pubmed , Xenbase
Kakebeen, More Than Just a Bandage: Closing the Gap Between Injury and Appendage Regeneration. 2019, Pubmed , Xenbase
Kakebeen, Chromatin accessibility dynamics and single cell RNA-Seq reveal new regulators of regeneration in neural progenitors. 2020, Pubmed , Xenbase
Kriegstein, The glial nature of embryonic and adult neural stem cells. 2009, Pubmed
Kuscha, Lesion-induced generation of interneuron cell types in specific dorsoventral domains in the spinal cord of adult zebrafish. 2012, Pubmed
Kuscha, Plasticity of tyrosine hydroxylase and serotonergic systems in the regenerating spinal cord of adult zebrafish. 2012, Pubmed
Langmead, Ultrafast and memory-efficient alignment of short DNA sequences to the human genome. 2009, Pubmed
Lee-Liu, Genome-wide expression profile of the response to spinal cord injury in Xenopus laevis reveals extensive differences between regenerative and non-regenerative stages. 2014, Pubmed , Xenbase
Lee-Liu, Spinal cord regeneration: lessons for mammals from non-mammalian vertebrates. 2013, Pubmed
Lee-Liu, The African clawed frog Xenopus laevis: A model organism to study regeneration of the central nervous system. 2017, Pubmed , Xenbase
Li, RSEM: accurate transcript quantification from RNA-Seq data with or without a reference genome. 2011, Pubmed
Love, Genome-wide analysis of gene expression during Xenopus tropicalis tadpole tail regeneration. 2011, Pubmed , Xenbase
Love, Amputation-induced reactive oxygen species are required for successful Xenopus tadpole tail regeneration. 2013, Pubmed , Xenbase
Marichal, Progenitors in the Ependyma of the Spinal Cord: A Potential Resource for Self-Repair After Injury. 2017, Pubmed
Marshall, Stage-dependent cardiac regeneration in Xenopus is regulated by thyroid hormone availability. 2019, Pubmed , Xenbase
Martinez-De Luna, Müller glia reactivity follows retinal injury despite the absence of the glial fibrillary acidic protein gene in Xenopus. 2017, Pubmed , Xenbase
Meletis, Spinal cord injury reveals multilineage differentiation of ependymal cells. 2008, Pubmed
Mescher, Changes in the inflammatory response to injury and its resolution during the loss of regenerative capacity in developing Xenopus limbs. 2013, Pubmed , Xenbase
Michel, Axonal-ependymal associations during early regeneration of the transected spinal cord in Xenopus laevis tadpoles. 1979, Pubmed , Xenbase
Mokalled, Injury-induced ctgfa directs glial bridging and spinal cord regeneration in zebrafish. 2016, Pubmed
Muñoz, Regeneration of Xenopus laevis spinal cord requires Sox2/3 expressing cells. 2015, Pubmed , Xenbase
Namiki, Cell proliferation and nestin expression in the ependyma of the adult rat spinal cord after injury. 1999, Pubmed
Norenberg, Fine structural localization of glutamine synthetase in astrocytes of rat brain. 1979, Pubmed
Ohsawa, Cell Extrusion: A Stress-Responsive Force for Good or Evil in Epithelial Homeostasis. 2018, Pubmed
O'Shea, Cell biology of spinal cord injury and repair. 2017, Pubmed
Parker, The Lesioned Spinal Cord Is a "New" Spinal Cord: Evidence from Functional Changes after Spinal Injury in Lamprey. 2017, Pubmed
Phipps, Model systems for regeneration: Xenopus. 2020, Pubmed , Xenbase
Reimer, Motor neuron regeneration in adult zebrafish. 2008, Pubmed
Sabelström, Resident neural stem cells restrict tissue damage and neuronal loss after spinal cord injury in mice. 2013, Pubmed
Sabourin, A mesenchymal-like ZEB1(+) niche harbors dorsal radial glial fibrillary acidic protein-positive stem cells in the spinal cord. 2009, Pubmed
Sefton, Electric Field Application In Vivo Regulates Neural Precursor Cell Behavior in the Adult Mammalian Forebrain. 2020, Pubmed
Shihabuddin, Adult spinal cord stem cells generate neurons after transplantation in the adult dentate gyrus. 2000, Pubmed
Silver, Regeneration beyond the glial scar. 2004, Pubmed
SIMS, Transection of the spinal cord in developing Xenopus laevis. 1962, Pubmed , Xenbase
Slack, The Xenopus tadpole: a new model for regeneration research. 2008, Pubmed , Xenbase
Sroga, Rats and mice exhibit distinct inflammatory reactions after spinal cord injury. 2003, Pubmed
Strand, Wnt/β-catenin signaling promotes regeneration after adult zebrafish spinal cord injury. 2016, Pubmed
Tapia, JAK-STAT pathway activation in response to spinal cord injury in regenerative and non-regenerative stages of Xenopus laevis. 2017, Pubmed , Xenbase
Tazaki, Salamander spinal cord regeneration: The ultimate positive control in vertebrate spinal cord regeneration. 2017, Pubmed
Thuret, Analysis of neural progenitors from embryogenesis to juvenile adult in Xenopus laevis reveals biphasic neurogenesis and continuous lengthening of the cell cycle. 2015, Pubmed , Xenbase
Tran, The Biology of Regeneration Failure and Success After Spinal Cord Injury. 2018, Pubmed
Tseng, Induction of vertebrate regeneration by a transient sodium current. 2010, Pubmed , Xenbase
Tsujioka, interleukin-11 induces and maintains progenitors of different cell lineages during Xenopus tadpole tail regeneration. 2017, Pubmed , Xenbase
Vígh, The system of cerebrospinal fluid-contacting neurons. Its supposed role in the nonsynaptic signal transmission of the brain. 2004, Pubmed
Wanner, Glial scar borders are formed by newly proliferated, elongated astrocytes that interact to corral inflammatory and fibrotic cells via STAT3-dependent mechanisms after spinal cord injury. 2013, Pubmed
Wehner, Wnt signaling controls pro-regenerative Collagen XII in functional spinal cord regeneration in zebrafish. 2017, Pubmed
Weiss, Multipotent CNS stem cells are present in the adult mammalian spinal cord and ventricular neuroaxis. 1996, Pubmed
Yu, clusterProfiler: an R package for comparing biological themes among gene clusters. 2012, Pubmed
Zhang, An RNA-sequencing transcriptome and splicing database of glia, neurons, and vascular cells of the cerebral cortex. 2014, Pubmed
Zhu, Electrical stimulation affects neural stem cell fate and function in vitro. 2019, Pubmed