Present address: Department of Metabolic Biology, John Innes Centre, Norwich Research Park, Colney, Norwich, NR4 7UH, UK.
Identification of SFR6, a key component in cold acclimation acting post-translationally on CBF function
Article first published online: 5 JAN 2009
© 2009 The Authors. Journal compilation © 2009 Blackwell Publishing Ltd
The Plant Journal
Volume 58, Issue 1, pages 97–108, April 2009
How to Cite
Knight, H., Mugford, S. G., Ülker, B., Gao, D., Thorlby, G. and Knight, M. R. (2009), Identification of SFR6, a key component in cold acclimation acting post-translationally on CBF function. The Plant Journal, 58: 97–108. doi: 10.1111/j.1365-313X.2008.03763.x
- Issue published online: 26 MAR 2009
- Article first published online: 5 JAN 2009
- Received 21 August 2008; revised 6 November 2008; accepted 20 November 2008; published online 5 January 2009.
- cold acclimation;
- C-box binding factor;
- freezing tolerance;
- COR genes
The sfr6-1 mutant of Arabidopsis thaliana was identified previously on the basis of its failure to undergo acclimation to freezing temperatures following exposure to low positive temperatures. This failure is attributed to a defect in the pathway leading to cold on-regulated (COR) gene expression via CBF (C-box binding factor) transcription factors. We identified a region of chromosome 4 containing SFR6 by positional mapping. Fine mapping of the sfr6-1 mutation proved impossible as the locus resides very close to the centromere. Therefore, we screened 380 T-DNA lines with insertions in genes within the large region to which sfr6-1 mapped. This resulted in the identification of two further mutant alleles of SFR6 (sfr6-2 and sfr6-3); like the original sfr6-1 mutation, these disrupt freezing tolerance and COR gene expression. To determine the protein sequence, we cloned an SFR6 cDNA based on the predicted coding sequence, but this offered no indication as to the mechanism by which SFR6 acts. The SFR6 gene itself is not strongly regulated by cold, thus discounting regulation of SFR6 activity at the transcriptional level. We show that over-expression of CBF1 or CBF2 transcription factors, which constitutively activate COR genes in the wild-type, cannot do so in sfr6-1. We demonstrate that CBF protein accumulates to wild-type levels in response to cold in sfr6-1. These results indicate a role for the SFR6 protein in the CBF pathway -downstream of CBF translation. The fact that the SFR6 protein is targeted to the nucleus may suggest a direct role in modulating gene expression.