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Volume 16, Number 14, Issue of July 15, 1996 pp. 4311-4321
Copyright ©1996 Society for Neuroscience

C-erbB2/neu Transfection Induces Gap Junctional Communication Incompetence in Glial Cells

Received Dec. 18, 1995; revised April 26, 1996; accepted April 29, 1996.

Andreas Hofer¹, Juan C. Sáez², Chia Cheng Chang³, James E. Trosko³, David C. Spray⁴, and Rolf Dermietzel¹

¹ Institute of Anatomy, University of Regensburg, 93053 Regensburg, Germany, ² Departamento de Ciencias Fisiologicas, Facultad de Ciences Biologicas, Pontificia Universidad Catholica de Chile, Santiago, Chile, ³ Department of Pediatrics and Human Development, Michigan State University, East Lansing, Michigan 48824, and ⁴ Albert Einstein College of Medicine, Department of Neuroscience, New York, New York 10461

Astrocytes form functional networks that participate in active signaling in which external stimuli are generated and amplified in many of the same ways as in neurons. Gap junctions between astrocytes offer the structural avenue by which the electrical and metabolic signals are propagated from one cell to another. Little is known about the trafficking, assembly, and degradation mechanisms of the major astrocytic gap junction protein connexin43. We have studied a glial cell line transfected with the C-erbB2/neu oncogene (neu⁺), finding severe interruption of gap junctional communication after stable transfection. Evidence from Western blotting and phosphorylation studies showed that the processing of connexin43 to its higher phosphorylated isoforms is disturbed. Confocal laser imaging indicates that the major deficit in the neu⁺ cells is attributable to a lack in plaque assembly of connexin43. Because the neu⁺ cells also lack N-CAM proteins and because work from others has indicated a close relationship between communication competence and constitutive CAM expression, our data suggest that expression of C-erbB2/neu oncogene alters cell-cell association via CAM proteins, which thereby affects gap junction plaque assembly and appropriate phosphorylation of connexin43.

Key words: gap junctions; astrocytes; oncogene; connexin43; phosphorylation; N-CAM

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