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Gene expression alterations in connexin null mice extend beyond the gap junction.
Dumitru A Iacobas1, Eliana Scemes, David C Spray
1Department of Neuroscience, Albert Einstein College of Medicine, Kennedy Center, Room 915C, 1300 Morris Park Ave, Bronx, NY 10461, USA.
Neurochemistry International
|May 18, 2004
Summary
Deleting Connexin43 (Cx43) gap junctions globally alters glial cell functions and disrupts nervous system development. This study reveals widespread gene expression changes in Cx43-deficient mice, impacting various cellular processes.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Connexin43 (Cx43) is a key gap junction protein in neonatal astrocytes and neural precursor cells.
- Understanding Cx43's role is crucial for comprehending nervous system development and function.
Purpose of the Study:
- To investigate the global effects of Cx43 gap junction gene expression on nervous system development and function.
- To compare gene expression patterns in wildtype and Cx43-deleted mice, including in disease models.
Main Methods:
- High-density mouse cDNA array studies were employed.
- Gene expression patterns were analyzed in cultured astrocytes and brains of wildtype and Cx43-deleted mice.
- Spinal cords from experimental autoimmune encephalomyelitis (EAE) mice were also examined.
Main Results:
- A significant number of genes showed statistically altered expression in mice with reduced Cx43 levels.
- Altered genes encode proteins involved in diverse cellular functions.
- Deletion of Cx43 resulted in globally altered glial functions beyond disrupted intercellular communication.
Conclusions:
- Cx43 deletion leads to widespread changes in glial cell function.
- Gap junction disruption has profound, global impacts on nervous system development and cellular processes.
- The study highlights the extensive role of Cx43 in maintaining normal nervous system function.