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  4. Olig3 Is Not Involved in the Ventral Patterning of Spinal Cord

Olig3 Is Not Involved in the Ventral Patterning of Spinal Cord

PLoS ONE, 2014 · DOI: 10.1371/journal.pone.0111076 · Published: October 28, 2014

NeurologyGenetics

Simple Explanation

This study investigates the role of the Olig3 gene in the development of the ventral spinal cord. Prior research indicated Olig3's involvement in dorsal spinal cord patterning. The researchers found that Olig3 is expressed in post-mitotic neurons in the ventral spinal cord and that its expression is regulated by the Nkx2.2 gene. However, they also discovered that Olig3 mutation doesn't significantly affect the generation or migration of ventral neurons, suggesting it plays a different role in ventral versus dorsal spinal cord development.

Study Duration
Not specified
Participants
Mouse and chick embryos
Evidence Level
Not specified

Key Findings

  • 1
    Olig3 is expressed in post-mitotic neurons in the ventral marginal zone of the developing spinal cord.
  • 2
    Nkx2.2 regulates the expression of Olig3 in V3 interneurons.
  • 3
    Olig3 mutation does not significantly affect the generation and migration of ventral neurons.

Research Summary

The study aimed to elucidate the function of Olig3 in ventral spinal cord development, contrasting its known role in the dorsal spinal cord. Results indicated that Olig3 is expressed in post-mitotic neurons in the ventral region, regulated by Nkx2.2, and does not affect the generation or migration of ventral neurons. These findings suggest distinct roles for Olig3 in the development of dorsal and ventral spinal cord.

Practical Implications

Understanding Spinal Cord Development

This research contributes to a deeper understanding of the complex genetic mechanisms that govern spinal cord development, particularly the differential roles of transcription factors like Olig3 in dorsal versus ventral patterning.

Future Research on Olig3 Function

The study suggests a need for further investigation into the specific functions of Olig3 in the ventral spinal cord, perhaps focusing on later differentiation events or morphogenesis of post-mitotic interneurons.

Potential Redundancy and Compensation

The lack of a significant effect from Olig3 mutation implies potential functional redundancy with other bHLH transcription factors, warranting exploration of these compensatory mechanisms.

Study Limitations

  • 1
    The study focuses primarily on the early stages of ventral spinal cord development.
  • 2
    The conventional Olig3 homozygous mouse die at birth due to the abnormal formation of respiratory center in the brainstem.
  • 3
    Potential functional redundancy from other bHLH transcription factors (e.g. Sim1?) that are similarly expressed in these ventral interneurons.

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