 |
|||||
|
|||||
|
|||||
|
|||||
|
|||||
The Journal of Neuroscience, June 1, 2003, 23(11):4549-4559
Previous Article | Next Article
Connexin 47 (Cx47)-Deficient Mice with Enhanced Green Fluorescent Protein Reporter Gene Reveal Predominant Oligodendrocytic Expression of Cx47 and Display Vacuolized Myelin in the CNS
Benjamin Odermatt,1 Kerstin Wellershaus,1 Anke Wallraff,3 Gerald Seifert,3 Joachim Degen,1 Carsten Euwens,1 Babette Fuss,4 Heinrich Büssow,2 Karl Schilling,2 Christian Steinhäuser,3 andKlaus Willecke1 1 Institut für Genetik, Universität Bonn, D-53117 Bonn, Germany, 2 Anatomisches Institut, Universität Bonn, D-53115 Bonn, Germany, 3 Experimentelle Neurobiologie, Neurochirurgie, Universität Bonn, D-53105 Bonn, Germany, and 4 Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia 23298
To further characterize the recently described gap junction gene connexin 47 (Cx47), we generated Cx47-null mice by replacing the Cx47 coding DNA with an enhanced green fluorescent protein (EGFP) reporter gene, which was thus placed under control of the endogenous Cx47 promoter. Homozygous mutant mice were fertile and showed no obvious morphological or behavioral abnormalities. Colocalization of EGFP fluorescence and immunofluorescence of cell marker proteins revealed that Cx47 was mainly expressed in oligodendrocytes in highly myelinated CNS tissues and in few calcium-binding protein S100
subunit-positive cells but not in neurons or peripheral sciatic nerve. This corrects our previous conclusion that Cx47 mRNA is expressed in brain and spinal cord neurons (Teubner et al., 2001). Cx47 protein was detected by Western blot analysis after immunoprecipitation in CNS tissues of wild-type mice but not in heart or Cx47-deficient tissues. Electron microscopic analysis of CNS white matter in Cx47-deficient mice revealed a conspicuous vacuolation of nerve fibers, particularly at the site of the optic nerve where axons are first contacted by oligodendrocytes and myelination starts. Initial analyses of Cx32/Cx47-double-deficient mice showed that these mice developed an action tremor and died on average at 51 d after birth. The central white matter of these double-deficient mice exhibited much more abundant vacuolation in nerve fibers than mice deficient only in Cx47.
Key words: EGFP; gap junctions; oligodendrocytes; glia cells; vacuolation; Cx32/Cx47 double-deficient mice
Received Jan. 2, 2003; revised Mar. 20, 2003; accepted Mar. 21, 2003.
This article has been cited by other articles:
S. E. Lutz, Y. Zhao, M. Gulinello, S. C. Lee, C. S. Raine, and C. F. Brosnan
Deletion of Astrocyte Connexins 43 and 30 Leads to a Dysmyelinating Phenotype and Hippocampal CA1 Vacuolation
J. Neurosci., June 17, 2009; 29(24): 7743 - 7752.
[Abstract] [Full Text] [PDF]
I. Sargiannidou, N. Vavlitou, S. Aristodemou, A. Hadjisavvas, K. Kyriacou, S. S. Scherer, and K. A. Kleopa
Connexin32 Mutations Cause Loss of Function in Schwann Cells and Oligodendrocytes Leading to PNS and CNS Myelination Defects
J. Neurosci., April 15, 2009; 29(15): 4736 - 4749.
[Abstract] [Full Text] [PDF]
J. L. Orthmann-Murphy, E. Salsano, C. K. Abrams, A. Bizzi, G. Uziel, M. M. Freidin, E. Lamantea, M. Zeviani, S. S. Scherer, and D. Pareyson
Hereditary spastic paraplegia is a novel phenotype for GJA12/GJC2 mutations
Brain, February 1, 2009; 132(2): 426 - 438.
[Abstract] [Full Text] [PDF]
J. L. Orthmann-Murphy, M. Freidin, E. Fischer, S. S. Scherer, and C. K. Abrams
Two Distinct Heterotypic Channels Mediate Gap Junction Coupling between Astrocyte and Oligodendrocyte Connexins
J. Neurosci., December 19, 2007; 27(51): 13949 - 13957.
[Abstract] [Full Text] [PDF]
J. Blanz, M. Schweizer, M. Auberson, H. Maier, A. Muenscher, C. A. Hubner, and T. J. Jentsch
Leukoencephalopathy upon Disruption of the Chloride Channel ClC-2
J. Neurosci., June 13, 2007; 27(24): 6581 - 6589.
[Abstract] [Full Text] [PDF]
D. M. Menichella, M. Majdan, R. Awatramani, D. A. Goodenough, E. Sirkowski, S. S. Scherer, and D. L. Paul
Genetic and Physiological Evidence That Oligodendrocyte Gap Junctions Contribute to Spatial Buffering of Potassium Released during Neuronal Activity
J. Neurosci., October 25, 2006; 26(43): 10984 - 10991.
[Abstract] [Full Text] [PDF]
M. Bugiani, S. Al Shahwan, E. Lamantea, A. Bizzi, E. Bakhsh, I. Moroni, M. R. Balestrini, G. Uziel, and M. Zeviani
GJA12 mutations in children with recessive hypomyelinating leukoencephalopathy
Neurology, July 25, 2006; 67(2): 273 - 279.
[Abstract] [Full Text] [PDF]
P. Bedner, H. Niessen, B. Odermatt, M. Kretz, K. Willecke, and H. Harz
Selective Permeability of Different Connexin Channels to the Second Messenger Cyclic AMP
J. Biol. Chem., March 10, 2006; 281(10): 6673 - 6681.
[Abstract] [Full Text] [PDF]
W. Tang, Y. Zhang, Q. Chang, S. Ahmad, I. Dahlke, H. Yi, P. Chen, D. L. Paul, and X. Lin
Connexin29 Is Highly Expressed in Cochlear Schwann Cells, and It Is Required for the Normal Development and Function of the Auditory Nerve of Mice
J. Neurosci., February 15, 2006; 26(7): 1991 - 1999.
[Abstract] [Full Text] [PDF]
S. Hidaka, Y. Akahori, and Y. Kurosawa
Dendrodendritic Electrical Synapses between Mammalian Retinal Ganglion Cells
J. Neurosci., November 17, 2004; 24(46): 10553 - 10567.
[Abstract] [Full Text] [PDF]
B. M. Altevogt and D. L. Paul
Four Classes of Intercellular Channels between Glial Cells in the CNS
J. Neurosci., May 5, 2004; 24(18): 4313 - 4323.
[Abstract] [Full Text] [PDF]
G. Cheron, D. Gall, L. Servais, B. Dan, R. Maex, and S. N. Schiffmann
Inactivation of Calcium-Binding Protein Genes Induces 160 Hz Oscillations in the Cerebellar Cortex of Alert Mice
J. Neurosci., January 14, 2004; 24(2): 434 - 441.
[Abstract] [Full Text] [PDF]
R. A. Taylor, E. M. Simon, H. G. Marks, and S. S. Scherer
The CNS phenotype of X-linked Charcot-Marie-Tooth disease: More than a peripheral problem
Neurology, December 9, 2003; 61(11): 1475 - 1478.
[Full Text] [PDF]
|
|
|
|
 |
|