Connexin 39.9 Protein Is Necessary for Coordinated Activation of Slow-twitch Muscle and Normal Behavior in Zebrafish
| Autor: | Koichi Kawakami, Louis Saint-Amant, Kazutoyo Ogino, John Y. Kuwada, Kazuhide Asakawa, Yuriko Naganawa, Yu Kawakami, Hiromi Hirata, Weibin Zhou, Kenta Yamada, Sean E. Low, Hua Wen, Akira Muto, Shawn M. Sprague, Wilson W. Cui |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Molecular Sequence Data
Mutation Missense Muscle Proteins Connexin In situ hybridization Biology Biochemistry Connexins medicine Animals Myocyte Molecular Biology Zebrafish Base Sequence Myogenesis Gap junction Gap Junctions Skeletal muscle Cell Biology Zebrafish Proteins biology.organism_classification Molecular biology Cell biology Electrophysiology Muscle Fibers Slow-Twitch medicine.anatomical_structure Gene Expression Regulation Developmental Biology |
| Zdroj: | Journal of Biological Chemistry. 287:1080-1089 |
| ISSN: | 0021-9258 |
| Popis: | In many tissues and organs, connexin proteins assemble between neighboring cells to form gap junctions. These gap junctions facilitate direct intercellular communication between adjoining cells, allowing for the transmission of both chemical and electrical signals. In rodents, gap junctions are found in differentiating myoblasts and are important for myogenesis. Although gap junctions were once believed to be absent from differentiated skeletal muscle in mammals, recent studies in teleosts revealed that differentiated muscle does express connexins and is electrically coupled, at least at the larval stage. These findings raised questions regarding the functional significance of gap junctions in differentiated muscle. Our analysis of gap junctions in muscle began with the isolation of a zebrafish motor mutant that displayed weak coiling at day 1 of development, a behavior known to be driven by slow-twitch muscle (slow muscle). We identified a missense mutation in the gene encoding Connexin 39.9. In situ hybridization found connexin 39.9 to be expressed by slow muscle. Paired muscle recordings uncovered that wild-type slow muscles are electrically coupled, whereas mutant slow muscles are not. The further examination of cellular activity revealed aberrant, arrhythmic touch-evoked Ca(2+) transients in mutant slow muscle and a reduction in the number of muscle fibers contracting in response to touch in mutants. These results indicate that Connexin 39.9 facilitates the spreading of neuronal inputs, which is irregular during motor development, beyond the muscle cells and that gap junctions play an essential role in the efficient recruitment of slow muscle fibers. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|