Semaphorin-6A controls guidance of corticospinal tract axons at multiple choice points

The corticospinal tract (CST) is a pathway in the nervous system that controls movement. This paper investigates how a molecule called Semaphorin-6A (Sema6A) affects the development of this pathway. Researchers studied mice with mutations in the Sema6A gene and found that the CST did not develop correctly. Specifically, axons (the long, slender projections of nerve cells) of the CST were misguided at key decision points in the brainstem. The findings suggest that Sema6A plays a critical role in guiding CST axons to their correct destinations during development. Understanding how Sema6A works could help in developing treatments for spinal cord injuries.

• 1
  Sema6A mutants exhibit hypoplasia and misrouting of the corticospinal tract, affecting the number of axons reaching the hindbrain and spinal cord.
• 2
  CST axons in Sema6A mutants display guidance defects at the mid-hindbrain boundary (MHB), including aberrant dorsal turns and midline crossing.
• 3
  PlxnA4 mutants exhibit a similar phenotype to Sema6A mutants in the caudal medulla, where CST axons fail to decussate properly, suggesting PlxnA4 is a receptor for Sema6A in this region.