First published online October 14, 2004
Development 131, 2103e (2004)
© The Company of Biologists Limited
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.
Related articles in Development:
- 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]
