Fgf-dependent glial cell bridges facilitate spinal cord regeneration in zebrafish

Yona Goldshmit, Tamar E Sztal, Patricia R Jusuf, Thomas E Hall, Mai Eva Nguyen Chi, Peter D Currie

Research output: Contribution to journalArticleResearchpeer-review

126 Citations (Scopus)

Abstract

Adult zebrafish show a remarkable capacity to regenerate their spinal column after injury, an ability that stands in stark contrast to the limited repair that occurs within the mammalian CNS post-injury. The reasons for this interspecies difference in regenerative capacity remain unclear. Here we demonstrate a novel role for Fgf signaling during glial cell morphogenesis in promoting axonal regeneration after spinal cord injury. Zebrafish glia are induced by Fgf signaling, to form an elongated bipolar morphology that forms a bridge between the two sides of the resected spinal cord, over which regenerating axons actively migrate. Loss of Fgf function inhibits formation of this glial bridge and prevents axon regeneration. Despite the poor potential for mammalian axonal regeneration, primate astrocytes activated by Fgf signaling adopt a similar morphology to that induced in zebrafish glia. This suggests that differential Fgf regulation, rather than intrinsic cell differences, underlie the distinct responses of mammalian and zebrafish glia to injury.
Original languageEnglish
Pages (from-to)7477 - 7492
Number of pages16
JournalJournal of Neuroscience
Volume32
Issue number22
DOIs
Publication statusPublished - 2012

Cite this

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title = "Fgf-dependent glial cell bridges facilitate spinal cord regeneration in zebrafish",
abstract = "Adult zebrafish show a remarkable capacity to regenerate their spinal column after injury, an ability that stands in stark contrast to the limited repair that occurs within the mammalian CNS post-injury. The reasons for this interspecies difference in regenerative capacity remain unclear. Here we demonstrate a novel role for Fgf signaling during glial cell morphogenesis in promoting axonal regeneration after spinal cord injury. Zebrafish glia are induced by Fgf signaling, to form an elongated bipolar morphology that forms a bridge between the two sides of the resected spinal cord, over which regenerating axons actively migrate. Loss of Fgf function inhibits formation of this glial bridge and prevents axon regeneration. Despite the poor potential for mammalian axonal regeneration, primate astrocytes activated by Fgf signaling adopt a similar morphology to that induced in zebrafish glia. This suggests that differential Fgf regulation, rather than intrinsic cell differences, underlie the distinct responses of mammalian and zebrafish glia to injury.",
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Fgf-dependent glial cell bridges facilitate spinal cord regeneration in zebrafish. / Goldshmit, Yona; Sztal, Tamar E; Jusuf, Patricia R; Hall, Thomas E; Nguyen Chi, Mai Eva; Currie, Peter D.

In: Journal of Neuroscience, Vol. 32, No. 22, 2012, p. 7477 - 7492.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Fgf-dependent glial cell bridges facilitate spinal cord regeneration in zebrafish

AU - Goldshmit, Yona

AU - Sztal, Tamar E

AU - Jusuf, Patricia R

AU - Hall, Thomas E

AU - Nguyen Chi, Mai Eva

AU - Currie, Peter D

PY - 2012

Y1 - 2012

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AB - Adult zebrafish show a remarkable capacity to regenerate their spinal column after injury, an ability that stands in stark contrast to the limited repair that occurs within the mammalian CNS post-injury. The reasons for this interspecies difference in regenerative capacity remain unclear. Here we demonstrate a novel role for Fgf signaling during glial cell morphogenesis in promoting axonal regeneration after spinal cord injury. Zebrafish glia are induced by Fgf signaling, to form an elongated bipolar morphology that forms a bridge between the two sides of the resected spinal cord, over which regenerating axons actively migrate. Loss of Fgf function inhibits formation of this glial bridge and prevents axon regeneration. Despite the poor potential for mammalian axonal regeneration, primate astrocytes activated by Fgf signaling adopt a similar morphology to that induced in zebrafish glia. This suggests that differential Fgf regulation, rather than intrinsic cell differences, underlie the distinct responses of mammalian and zebrafish glia to injury.

UR - http://www.jneurosci.org/content/32/22/7477.full.pdf

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DO - 10.1523/JNEUROSCI.0758-12.2012

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JF - Journal of Neuroscience

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