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First published online October 14, 2004

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The zebrafish that can't relax

During muscle contraction, Ca²⁺ released from the sarco(endo)plasmic reticulum (SER) into the cytosol activates actin/myosin sliding. It is then rapidly pumped out of the cytosol by the SER Ca²⁺ ATPase 1 (SERCA1) to allow muscle relaxation. On p. 5457, Hirata and colleagues report that this muscle relaxation does not occur in the zebrafish behavioural mutant accordion (acc). Twenty-four hours post-fertilisation, zebrafish embryos respond to touch by rapidly coiling their tails once each way; acc mutant embryos respond with a bilateral contraction of trunk muscles, which shortens their trunks. Although nerve transmission is normal in these mutants, the cytosolic Ca²⁺ decay in their muscles is very slow, preventing their muscles from relaxing normally. This defect is due to a mutation in the atp2a1 gene, which encodes SERCA1, making the acc mutant an attractive model in which to study Brody disease, a human motor disorder caused by SERCA1 mutations.

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accordion, a zebrafish behavioral mutant, has a muscle relaxation defect due to a mutation in the ATPase Ca²⁺ pump SERCA1

Hiromi Hirata, Louis Saint-Amant, Julie Waterbury, Wilson Cui, Weibin Zhou, Qin Li, Daniel Goldman, Michael Granato, and John Y. Kuwada
Development 2004 131: 5457-5468. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?