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Mirk/Dyrk1B controls ventral spinal cord development via Shh pathway. | LitMetric

Mirk/Dyrk1B controls ventral spinal cord development via Shh pathway.

Cell Mol Life Sci

Laboratory of Cellular and Molecular Neurobiology-Stem Cells, Hellenic Pasteur Institute, Athens, Greece.

Published: January 2024

AI Article Synopsis

  • This study investigates the role of Dyrk1B kinase in regulating neuron types in the developing chick spinal cord through the Sonic hedgehog (Shh) signaling pathway.
  • It finds that overexpressing Dyrk1B decreases the number of ventral progenitors and motor neurons, while inhibiting Dyrk1B leads to an increase in these cells.
  • The research suggests that targeting Dyrk1B could be a potential therapeutic strategy for treating motor neuron diseases by modulating the Shh/Gli pathway.

Article Abstract

Cross-talk between Mirk/Dyrk1B kinase and Sonic hedgehog (Shh)/Gli pathway affects physiology and pathology. Here, we reveal a novel role for Dyrk1B in regulating ventral progenitor and neuron subtypes in the embryonic chick spinal cord (SC) via the Shh pathway. Using in ovo gain-and-loss-of-function approaches at E2, we report that Dyrk1B affects the proliferation and differentiation of neuronal progenitors at E4 and impacts on apoptosis specifically in the motor neuron (MN) domain. Especially, Dyrk1B overexpression decreases the numbers of ventral progenitors, MNs, and V2a interneurons, while the pharmacological inhibition of endogenous Dyrk1B kinase activity by AZ191 administration increases the numbers of ventral progenitors and MNs. Mechanistically, Dyrk1B overexpression suppresses Shh, Gli2 and Gli3 mRNA levels, while conversely, Shh, Gli2 and Gli3 transcription is increased in the presence of Dyrk1B inhibitor AZ191 or Smoothened agonist SAG. Most importantly, in phenotype rescue experiments, SAG restores the Dyrk1B-mediated dysregulation of ventral progenitors. Further at E6, Dyrk1B affects selectively the medial lateral motor neuron column (LMCm), consistent with the expression of Shh in this region. Collectively, these observations reveal a novel regulatory function of Dyrk1B kinase in suppressing the Shh/Gli pathway and thus affecting ventral subtypes in the developing spinal cord. These data render Dyrk1B a possible therapeutic target for motor neuron diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10830675PMC
http://dx.doi.org/10.1007/s00018-023-05097-9DOI Listing

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