Limits...
Semaphorin signaling in vertebrate neural circuit assembly.

Yoshida Y - Front Mol Neurosci (2012)

Bottom Line: The major semaphorin receptors are plexins and neuropilins, however other receptors and co-receptors also mediate signaling by semaphorins.Upon semaphorin binding to their receptors, downstream signaling molecules transduce this event within cells to mediate further events, including alteration of microtubule and actin cytoskeletal dynamics.Here, I review recent studies on semaphorin signaling in vertebrate neural circuit assembly, with the goal of highlighting how this diverse family of cues and receptors imparts exquisite specificity to neural complex connectivity.

View Article: PubMed Central - PubMed

Affiliation: Division of Developmental Biology, Cincinnati Children's Hospital Medical Center Cincinnati, OH, USA.

ABSTRACT
Neural circuit formation requires the coordination of many complex developmental processes. First, neurons project axons over long distances to find their final targets and then establish appropriate connectivity essential for the formation of neuronal circuitry. Growth cones, the leading edges of axons, navigate by interacting with a variety of attractive and repulsive axon guidance cues along their trajectories and at final target regions. In addition to guidance of axons, neuronal polarization, neuronal migration, and dendrite development must be precisely regulated during development to establish proper neural circuitry. Semaphorins consist of a large protein family, which includes secreted and cell surface proteins, and they play important roles in many steps of neural circuit formation. The major semaphorin receptors are plexins and neuropilins, however other receptors and co-receptors also mediate signaling by semaphorins. Upon semaphorin binding to their receptors, downstream signaling molecules transduce this event within cells to mediate further events, including alteration of microtubule and actin cytoskeletal dynamics. Here, I review recent studies on semaphorin signaling in vertebrate neural circuit assembly, with the goal of highlighting how this diverse family of cues and receptors imparts exquisite specificity to neural complex connectivity.

No MeSH data available.


Sema6D controls retinal midline crossing through its interaction with PlexA1 and Nr-CAM. Sema6D and Nr-CAM are expressed by glial cells in the chiasm, and PlexA1 is expressed by SSEA1+ neurons in the chiasm. Nr-CAM and PlexA1 are expressed by crossed RGCs. The receptor complex in cis on RGCs and Sema6D alone leads to repulsion of RGCs, whereas the complex on chiasm cells acting in trans with RGC receptors promotes axonal attraction.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3368236&req=5

Figure 2: Sema6D controls retinal midline crossing through its interaction with PlexA1 and Nr-CAM. Sema6D and Nr-CAM are expressed by glial cells in the chiasm, and PlexA1 is expressed by SSEA1+ neurons in the chiasm. Nr-CAM and PlexA1 are expressed by crossed RGCs. The receptor complex in cis on RGCs and Sema6D alone leads to repulsion of RGCs, whereas the complex on chiasm cells acting in trans with RGC receptors promotes axonal attraction.

Mentions: A very recent study demonstrates that Sema6D thorough its receptors PlexA1 and Nr-CAM promotes retinal axon midline crossing (Kuwajima et al., 2012). The authors found that Sema6D and Nr-CAM are expressed on midline radial glia and PlexA1 on chiasm neurons, and PlexA1 and Nr-CAM are expressed on contralateral RGCs. A series of sophisticated in vitro culture experiments reveal that both PlexA1 and Nr-CAM are required on crossed RGCs for inhibition by Sema6D alone, whereas Sema6D interacting together with PlexA1 and Nr-CAM promotes growth (Kuwajima et al., 2012). Furthermore, they found that Nr-CAM can interact with both Sema6D and PlexA1. Finally, in the absence of Sema6D or both PlexA1 and Nr-CAM in vivo, RGC axons defasciculate, misroute into the caudal diencephalon, and more frequently project into the ipsilateral optic tract (Kuwajima et al., 2012). This study provides a novel mechanism underling midline crossing: accessory recognition proteins expressed by ligand-expressing cells modulate ligand activity. This strategy allows a switch in ligand activity without changing receptor expression on responsive axons (Figure 2).


Semaphorin signaling in vertebrate neural circuit assembly.

Yoshida Y - Front Mol Neurosci (2012)

Sema6D controls retinal midline crossing through its interaction with PlexA1 and Nr-CAM. Sema6D and Nr-CAM are expressed by glial cells in the chiasm, and PlexA1 is expressed by SSEA1+ neurons in the chiasm. Nr-CAM and PlexA1 are expressed by crossed RGCs. The receptor complex in cis on RGCs and Sema6D alone leads to repulsion of RGCs, whereas the complex on chiasm cells acting in trans with RGC receptors promotes axonal attraction.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3368236&req=5

Figure 2: Sema6D controls retinal midline crossing through its interaction with PlexA1 and Nr-CAM. Sema6D and Nr-CAM are expressed by glial cells in the chiasm, and PlexA1 is expressed by SSEA1+ neurons in the chiasm. Nr-CAM and PlexA1 are expressed by crossed RGCs. The receptor complex in cis on RGCs and Sema6D alone leads to repulsion of RGCs, whereas the complex on chiasm cells acting in trans with RGC receptors promotes axonal attraction.
Mentions: A very recent study demonstrates that Sema6D thorough its receptors PlexA1 and Nr-CAM promotes retinal axon midline crossing (Kuwajima et al., 2012). The authors found that Sema6D and Nr-CAM are expressed on midline radial glia and PlexA1 on chiasm neurons, and PlexA1 and Nr-CAM are expressed on contralateral RGCs. A series of sophisticated in vitro culture experiments reveal that both PlexA1 and Nr-CAM are required on crossed RGCs for inhibition by Sema6D alone, whereas Sema6D interacting together with PlexA1 and Nr-CAM promotes growth (Kuwajima et al., 2012). Furthermore, they found that Nr-CAM can interact with both Sema6D and PlexA1. Finally, in the absence of Sema6D or both PlexA1 and Nr-CAM in vivo, RGC axons defasciculate, misroute into the caudal diencephalon, and more frequently project into the ipsilateral optic tract (Kuwajima et al., 2012). This study provides a novel mechanism underling midline crossing: accessory recognition proteins expressed by ligand-expressing cells modulate ligand activity. This strategy allows a switch in ligand activity without changing receptor expression on responsive axons (Figure 2).

Bottom Line: The major semaphorin receptors are plexins and neuropilins, however other receptors and co-receptors also mediate signaling by semaphorins.Upon semaphorin binding to their receptors, downstream signaling molecules transduce this event within cells to mediate further events, including alteration of microtubule and actin cytoskeletal dynamics.Here, I review recent studies on semaphorin signaling in vertebrate neural circuit assembly, with the goal of highlighting how this diverse family of cues and receptors imparts exquisite specificity to neural complex connectivity.

View Article: PubMed Central - PubMed

Affiliation: Division of Developmental Biology, Cincinnati Children's Hospital Medical Center Cincinnati, OH, USA.

ABSTRACT
Neural circuit formation requires the coordination of many complex developmental processes. First, neurons project axons over long distances to find their final targets and then establish appropriate connectivity essential for the formation of neuronal circuitry. Growth cones, the leading edges of axons, navigate by interacting with a variety of attractive and repulsive axon guidance cues along their trajectories and at final target regions. In addition to guidance of axons, neuronal polarization, neuronal migration, and dendrite development must be precisely regulated during development to establish proper neural circuitry. Semaphorins consist of a large protein family, which includes secreted and cell surface proteins, and they play important roles in many steps of neural circuit formation. The major semaphorin receptors are plexins and neuropilins, however other receptors and co-receptors also mediate signaling by semaphorins. Upon semaphorin binding to their receptors, downstream signaling molecules transduce this event within cells to mediate further events, including alteration of microtubule and actin cytoskeletal dynamics. Here, I review recent studies on semaphorin signaling in vertebrate neural circuit assembly, with the goal of highlighting how this diverse family of cues and receptors imparts exquisite specificity to neural complex connectivity.

No MeSH data available.