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The Journal of Neuroscience, November 26, 2003, 23(34):10963-10970

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Development/Plasticity/Repair
Corpus Callosum Deficiency in Transgenic Mice Expressing a Truncated Ephrin-A Receptor

Zhaoliang Hu,^1,3 Xin Yue,^1,3 Guanfang Shi,^1,3 Yong Yue,^1,3 David P. Crockett,³ Jan Blair-Flynn,⁴ Kenneth Reuhl,² Lino Tessarollo,⁴ and Renping Zhou^1,3

¹Laboratory for Cancer Research and ²Department of Pharmacology, College of Pharmacy, Rutgers University, and ³Department of Neuroscience and Cell Biology, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, and ⁴Neural Development Group, Mouse Cancer Genetics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21701

The A-class of the erythropoietin-producing hepatocellular carcinoma cell-derived (EphA) tyrosine kinase receptors and their ligands, the A-ephrins, play critical roles in the specification of topographic axon projection maps during development. In this study, the role of the EphA subfamily in callosal projections was investigated using transgenic mice expressing a kinase deletion mutant of EphA5. In approximately half of these transgenic mice, cerebral cortical neurons in various cortical regions (primary and secondary somatosensory cortices and frontal as well as visual areas) failed to project to the contralateral cortex. When commissural axons were examined with DiI labeling, few callosal fibers were found to traverse the midline in both the adult and neonatal transgenic mice. This defect in callosal development correlates with the expression of the transgene, because neurons in the superficial layers of the motor cortex, where transgene expression is low, show normal contralateral projection through the corpus callosum. In addition, multiple EphA receptors are expressed in callosal neurons and ephrin-A5 stimulates neurite outgrowth of callosal neurons in vitro. The midline glia structures important for callosal axon midline crossing appear normal in the transgenic mice, suggesting that the defects are unrelated to defective guidance structures at the midline. These observations suggest critical functions for EphA receptor in establishing callosal connections during brain development.

Key words: corpus callosum; axon guidance; Eph receptors; ephrins; transgenic mice; neurite outgrowth

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Received Aug 20, 2003; revised September 26, 2003; accepted September 26, 2003.

This article has been cited by other articles:

				H. A. North, X. Zhao, S. M. Kolk, M. A. Clifford, D. M. Ziskind, and M. J. Donoghue Promotion of proliferation in the developing cerebral cortex by EphA4 forward signaling Development, July 15, 2009; 136(14): 2467 - 2476. [Abstract] [Full Text] [PDF]

				J. O. Bush and P. Soriano Ephrin-B1 regulates axon guidance by reverse signaling through a PDZ-dependent mechanism Genes & Dev., July 1, 2009; 23(13): 1586 - 1599. [Abstract] [Full Text] [PDF]

				T. M. Coate, J. A. Wirz, and P. F. Copenhaver Reverse Signaling via a Glycosyl-Phosphatidylinositol-Linked Ephrin Prevents Midline Crossing by Migratory Neurons during Embryonic Development in Manduca J. Neurosci., April 9, 2008; 28(15): 3846 - 3860. [Abstract] [Full Text] [PDF]

				F. Tovar-Moll, J. Moll, R. de Oliveira-Souza, I. Bramati, P. A. Andreiuolo, and R. Lent Neuroplasticity in Human Callosal Dysgenesis: A Diffusion Tensor Imaging Study Cereb Cortex, March 1, 2007; 17(3): 531 - 541. [Abstract] [Full Text] [PDF]

				S. W. Mendes, M. Henkemeyer, and D. J. Liebl Multiple Eph Receptors and B-Class Ephrins Regulate Midline Crossing of Corpus Callosum Fibers in the Developing Mouse Forebrain J. Neurosci., January 18, 2006; 26(3): 882 - 892. [Abstract] [Full Text] [PDF]

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