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  Myostatin is a negative regulator of adult neurogenesis after spinal cord injury in zebrafish

Saraswathy, V. M., Zhou, L., McAdow, A. R., Burris, B., Dogra, D., Reischauer, S., et al. (2022). Myostatin is a negative regulator of adult neurogenesis after spinal cord injury in zebrafish. CELL REPORTS, 41(8): 111705. doi:10.1016/j.celrep.2022.111705.

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Saraswathy, Vishnu Muraleedharan, Autor
Zhou, Lili, Autor
McAdow, Anthony R., Autor
Burris, Brooke, Autor
Dogra, Deepika1, Autor           
Reischauer, Sven1, Autor           
Mokalled, Mayssa H., Autor
Affiliations:
1Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591697              

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 Zusammenfassung: Intrinsic and extrinsic inhibition of neuronal regeneration obstruct spinal cord (SC) repair in mammals. In contrast, adult zebrafish achieve functional recovery after complete SC transection. While studies of innate SC regeneration have focused on axon regrowth as a primary repair mechanism, how local adult neurogen-esis affects functional recovery is unknown. Here, we uncover dynamic expression of zebrafish myostatin b (mstnb) in a niche of dorsal SC progenitors after injury. mstnb mutants show impaired functional recovery, normal glial and axonal bridging across the lesion, and an increase in the profiles of newborn neurons. Molec-ularly, neuron differentiation genes are upregulated, while the neural stem cell maintenance gene fgf1b is downregulated in mstnb mutants. Finally, we show that human fibroblast growth factor 1 (FGF1) treatment rescues the molecular and cellular phenotypes of mstnb mutants. These studies uncover unanticipated neurogenic functions formstnb and establish the importance of local adult neurogenesis for innate SC repair.

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 Datum: 2022-11-22
 Publikationsstatus: Online veröffentlicht
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 Ort, Verlag, Ausgabe: -
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 Identifikatoren: ISI: 000892121000007
DOI: 10.1016/j.celrep.2022.111705
PMID: 36417881
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Titel: CELL REPORTS
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 41 (8) Artikelnummer: 111705 Start- / Endseite: - Identifikator: ISSN: 2211-1247