A Chemical Genetic Approach Reveals Distinct Mechanisms of EphB Signaling During Brain Development

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A Chemical Genetic Approach Reveals Distinct Mechanisms of EphB Signaling During Brain Development

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Title: A Chemical Genetic Approach Reveals Distinct Mechanisms of EphB Signaling During Brain Development
Author: Soskis, Michael J.; Ho, Hsin-Yi Henry; Bloodgood, Brenda L.; Robichaux, Michael A.; Malik, Athar N.; Ataman, Bulent; Rubin, Alex A.; Zieg, Janine; Zhang, Chao; Shokat, Kevan M.; Sharma, Nikhil; Cowan, Christopher W.; Greenberg, Michael E.

Note: Order does not necessarily reflect citation order of authors.

Citation: Soskis, M. J., H. H. Ho, B. L. Bloodgood, M. A. Robichaux, A. N. Malik, B. Ataman, A. A. Rubin, et al. 2012. “A Chemical Genetic Approach Reveals Distinct Mechanisms of EphB Signaling During Brain Development.” Nature neuroscience 15 (12): 1645-1654. doi:10.1038/nn.3249. http://dx.doi.org/10.1038/nn.3249.
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Abstract: EphB receptor tyrosine kinases control multiple steps in nervous system development. However, it remains unclear whether EphBs regulate these different developmental processes directly or indirectly. In addition, as EphBs signal through multiple mechanisms, it has been challenging to define which signaling functions of EphBs regulate particular developmental events. To address these issues, we engineered triple knockin mice in which the kinase activity of three neuronally expressed EphBs can be rapidly, reversibly, and specifically blocked. Using these mice we demonstrate that the tyrosine kinase activity of EphBs is required for axon guidance in vivo. By contrast, EphB-mediated synaptogenesis occurs normally when the kinase activity of EphBs is inhibited suggesting that EphBs mediate synapse development by an EphB tyrosine kinase-independent mechanism. Taken together, these experiments reveal that EphBs control axon guidance and synaptogenesis by distinct mechanisms, and provide a new mouse model for dissecting EphB function in development and disease.
Published Version: doi:10.1038/nn.3249
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509236/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11708549
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