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Abstract
Ephrins and Eph receptors enable contact-mediated interactions between cells at every stage of nervous system development. In spite of their broad binding affinities, Eph proteins facilitate specificity in neuronal migration and axon targeting. This review focuses on recent studies that demonstrate how these proteins interact with each other, and with other signaling pathways, to guide specificity in a diverse set of developmental processes.
Highlights
The complexity of nervous system function reflects a vast underlying diversity of neuronal cells and their integration in precise circuitry
Multiple modes of Eph-ephrin signaling provide combinatorial codes that differentiate between groups of cells and coordinate multiple aspects of neural development, including cell migration and axon targeting
The authors overexpressed the zinc finger transcription factor Zic[2], which is expressed in retinal ganglion cells and which activates EphB1 and regulates numerous other genes as well. They found that early exogenous expression of Zic[2] was significantly more effective at inducing ipsilateral projections than EphB1, consistent with the view that a network of genes is needed to balance responses to ipsilateral versus contralateral cues. The identification of these genes and the integration of their roles in target selection, which may require a computational modeling approach, will greatly facilitate our understanding of how Eph-ephrin signaling leads to precision in axon targeting
Summary
The complexity of nervous system function reflects a vast underlying diversity of neuronal cells and their integration in precise circuitry. They found that early exogenous expression of Zic[2] was significantly more effective at inducing ipsilateral projections than EphB1, consistent with the view that a network of genes is needed to balance responses to ipsilateral versus contralateral cues The identification of these genes and the integration of their roles in target selection, which may require a computational modeling approach, will greatly facilitate our understanding of how Eph-ephrin signaling leads to precision in axon targeting. Abnormal glial proliferation at the midline in mutant mice brains suggested that Eph family proteins regulate this population through growth suppression[54] These studies suggest that agenesis of the corpus callosum in CFNS results from defects in axon guidance regulated by Eph-ephrin signaling. Grant information Research in the laboratory of KSC is supported by NIH R01DC010796
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