Expression of thioredoxin-1 in the ASJ neuron corresponds with and enhances intrinsic regenerative capacity under lesion conditioning in C. elegans.

Autor: Grooms NWF; Department of Bioengineering, Northeastern University, Boston, Massachusetts, USA., Fitzgerald MQ; Department of Bioengineering, Northeastern University, Boston, Massachusetts, USA., Zuckerman B; Gladstone/UCSF Center for Cell Circuitry, Gladstone Institutes, San Francisco, California, USA., Ureña SE; Department of Bioengineering, Northeastern University, Boston, Massachusetts, USA., Weinberger LS; Gladstone/UCSF Center for Cell Circuitry, Gladstone Institutes, San Francisco, California, USA., Chung SH; Department of Bioengineering, Northeastern University, Boston, Massachusetts, USA.
Jazyk: angličtina
Zdroj: FEBS letters [FEBS Lett] 2023 Jul; Vol. 597 (14), pp. 1880-1893. Date of Electronic Publication: 2023 Jun 19.
DOI: 10.1002/1873-3468.14684
Abstrakt: A conditioning lesion of the peripheral sensory axon triggers robust central axon regeneration in mammals. We trigger conditioned regeneration in the Caenorhabditis elegans ASJ neuron by laser surgery or genetic disruption of sensory pathways. Conditioning upregulates thioredoxin-1 (trx-1) expression, as indicated by trx-1 promoter-driven expression of green fluorescent protein and fluorescence in situ hybridization (FISH), suggesting trx-1 levels and associated fluorescence indicate regenerative capacity. The redox activity of trx-1 functionally enhances conditioned regeneration, but both redox-dependent and -independent activity inhibit non-conditioned regeneration. Six strains isolated in a forward genetic screen for reduced fluorescence, which suggests diminished regenerative potential, also show reduced axon outgrowth. We demonstrate an association between trx-1 expression and the conditioned state that we leverage to rapidly assess regenerative capacity.
(© 2023 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)
Databáze: MEDLINE
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