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The Journal of Neuroscience, April 22, 2009, 29(16):5207-5217; doi:10.1523/JNEUROSCI.0637-09.2009

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Cellular/Molecular
Caenorhabditis elegans Innexins Regulate Active Zone Differentiation

Edward Yeh,^1 * Taizo Kawano,^1 * Sharon Ng,^1,2 * Richard Fetter,³ Wesley Hung,¹ Ying Wang,¹ and Mei Zhen^1,2

¹Samuel Lunenfeld Research Institute, Montana Sinai Hospital, Toronto, Ontario M5G 1X5, Canada, ²Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada, and ³Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10021

Correspondence should be addressed to Mei Zhen, Samuel Lunenfeld Research Institute, Montana Sinai Hospital, Toronto, ON M5G 1X5, Canada. Email: zhen{at}mshri.on.ca

In a genetic screen for active zone defective mutants in Caenorhabditis elegans, we isolated a loss-of-function allele of unc-7, a gene encoding an innexin/pannexin family gap junction protein. Innexin UNC-7 regulates the size and distribution of active zones at C. elegans neuromuscular junctions. Loss-of-function mutations in another innexin, UNC-9, cause similar active zone defects as unc-7 mutants. In addition to presumptive gap junction localizations, both UNC-7 and UNC-9 are also localized perisynaptically throughout development and required in presynaptic neurons to regulate active zone differentiation. Our mosaic analyses, electron microscopy, as well as expression studies suggest a novel and likely nonjunctional role of specific innexins in active zone differentiation in addition to gap junction formations.

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Received Feb. 6, 2009; revised March 13, 2009; accepted March 16, 2009.

Correspondence should be addressed to Mei Zhen, Samuel Lunenfeld Research Institute, Montana Sinai Hospital, Toronto, ON M5G 1X5, Canada. Email: zhen{at}mshri.on.ca

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