Originally published as Genetics Published Articles Ahead of Print on March 21, 2005.

Genetics, Vol. 170, 387-400, May 2005, Copyright © 2005
doi:10.1534/genetics.104.035238

Natural Allelic Variation in the Temperature-Compensation Mechanisms of the Arabidopsis thaliana Circadian Clock

* Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, United Kingdom
§ Interdisciplinary Programme for Cellular Regulation, University of Warwick, Coventry CV4 7AL, United Kingdom
{dagger} Warwick HRI, Wellesbourne, Warwick CV35 9EF, United Kingdom
{ddagger} Biological Research Centre of the Hungarian Academy of Sciences, Szeged H-6723, Hungary

1 Corresponding author: Department of Biological Sciences, University of Warwick, Gibbet Hill Rd., Coventry CV4 7AL, United Kingdom.
E-mail: andrew.millar{at}ed.ac.uk

Temperature compensation is a defining feature of circadian oscillators, yet no components contributing to the phenomenon have been identified in plants. We tested 27 accessions of Arabidopsis thaliana for circadian leaf movement at a range of constant temperatures. The accessions showed varying patterns of temperature compensation, but no clear associations to the geographic origin of the accessions could be made. Quantitative trait loci (QTL) were mapped for period and amplitude of leaf movement in the Columbia by Landsberg erecta (CoL) and Cape Verde Islands by Landsberg erecta (CvL) recombinant inbred lines (RILs) at 12°, 22°, and 27°. Six CvL and three CoL QTL were located for circadian period. All of the period QTL were temperature specific, suggesting that they may be involved in temperature compensation. The flowering-time gene GIGANTEA and F-box protein ZEITLUPE were identified as strong candidates for two of the QTL on the basis of mapping in near isogenic lines (NILs) and sequence comparison. The identity of these and other candidates suggests that temperature compensation is not wholly determined by the intrinsic properties of the central clock proteins in Arabidopsis, but rather by other genes that act in trans to alter the regulation of these core proteins.




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