Skip to main content

Free Content Calmodulin binds to inv protein: Implication for the regulation of inv function

Download Article:

The full text article is temporarily unavailable.

We apologise for the inconvenience. Please try again later.

Establishment of the left–right asymmetry of internal organs is essential for the normal development of vertebrates. The inv mutant in mice shows a constant reversal of left–right asymmetry and although the inv gene has been cloned, its biochemical and cell biological functions have not been defined. Here, we show that calmodulin binds to mouse inv protein at two sites (IQ1 and IQ2). The binding of calmodulin to the IQ2 site occurs in the absence of Ca2+ and is not observed in the presence of Ca2+. Injection of mouse inv mRNA into the right blastomere of Xenopus embryos at the two-cell stage randomized the left–right asymmetry of the embryo and altered the patterns of Xnr-1 and Pitx2 expression. Importantly, inv mRNA that lacked the region encoding the IQ2 site was unable to randomize left–right asymmetry in Xenopus embryos, implying that the IQ2 site is essential for inv to randomize left–right asymmetry in Xenopus. These results suggest that calmodulin binding may regulate inv function. Based on our findings, we propose a model for the regulation of inv function by calcium–calmodulin and discuss its implications.
No References
No Citations
No Supplementary Data
No Data/Media
No Metrics

Keywords: Xenopus laevis; calcium; calmodulin; inv; left–right asymmetry

Document Type: Research Article

Publication date: 2001-12-01

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more