The central
and peripheral nervous systems of vertebrates are partitioned at specific
points within the spinal cord, ensuring that the cell bodies of neurons from
each system are not mixed, while still allowing axons to be connected. Previous
studies have identified a transient population of cells responsible for this
partitioning, termed boundary cap cells. The molecular mechanism of boundary
cap formation and function is discussed in a recent minireview for Journal of
Biology by Sophie Chauvet and Geneviève Rougon, highlighting two
interesting studies published in Neural Development, which
illustrate a role for semaphorin-plexin signaling in this process.

The role of
semaphorin 6A (Sema6A) was determined by Bron et al.
through the study of chick and mouse embryos deficient in either Semaphorin 6A
or neuropilin-2. This study illustrates the importance of the interaction
between these two molecules in preventing the exit of motor neuron cell bodies
from the spinal cord, and identifies Plexin-A2 as a putative interacting
partner in this signaling pathway. Using RNA interference, Bron et al.
also demonstrate that MICAL3, expressed by motor neurons, is an essential
downstream component of this signaling pathway in chick.

In a
related study, Mauti et
al. showed that depletion of Sema6A expression leads to the
ectopic migration of motor neuron cell bodies, a phenotype mimicking the
ablation of boundary cap cells. In contrast to the study by Bron et al.,
the authors identified Plexin-A1 or Plexin-A4, and not Plexin-A2, as
candidate interacting molecules in this process. These important findings are
discussed in the literature evaluation service, Faculty
of 1000 (Biology).

In
conjunction, these studies shed new light on the role of extracellular cues in
establishing the positional identity of developing neuronal circuits. While the
minireview in Journal of Biology highlights the important advance
resulting from combining these findings, it also discusses the interesting
discrepancies between the two studies.