Gene expression profiles of Arabidopsis Cvi seeds during dormancy cycling indicate a common underlying dormancy control mechanism
Article first published online: 4 MAY 2006
The Plant Journal
Volume 46, Issue 5, pages 805–822, June 2006
How to Cite
Cadman, C. S.C., Toorop, P. E., Hilhorst, H. W.M. and Finch-Savage, W. E. (2006), Gene expression profiles of Arabidopsis Cvi seeds during dormancy cycling indicate a common underlying dormancy control mechanism. The Plant Journal, 46: 805–822. doi: 10.1111/j.1365-313X.2006.02738.x
- Issue published online: 4 MAY 2006
- Article first published online: 4 MAY 2006
- Received 2 December 2005; revised 10 February 2006; accepted 17 February 2006.
Vol. 47, Issue 1, 164, Article first published online: 12 JUN 2006
- seed dormancy;
- dormancy cycling;
- transcriptome analysis;
- abscisic acid;
- gibberellic acid
Physiologically dormant seeds, like those of Arabidopsis, will cycle through dormant states as seasons change until the environment is favourable for seedling establishment. This phenomenon is widespread in the plant kingdom, but has not been studied at the molecular level. Full-genome microarrays were used for a global transcript analysis of Arabidopsis thaliana (accession Cvi) seeds in a range of dormant and dry after-ripened states during cycling. Principal component analysis of the expression patterns observed showed that they differed in newly imbibed primary dormant seeds, as commonly used in experimental studies, compared with those in the maintained primary and secondary dormant states that exist during cycling. Dormant and after-ripened seeds appear to have equally active although distinct gene expression programmes, dormant seeds having greatly reduced gene expression associated with protein synthesis, potentially controlling the completion of germination. A core set of 442 genes were identified that had higher expression in all dormant states compared with after-ripened states. Abscisic acid (ABA) responsive elements were significantly over-represented in this set of genes the expression of which was enhanced when multiple copies of the elements were present. ABA regulation of dormancy was further supported by expression patterns of key genes in ABA synthesis/catabolism, and dormancy loss in the presence of fluridone. The data support an ABA–gibberelic acid hormone balance mechanism controlling cycling through dormant states that depends on synthetic and catabolic pathways of both hormones. Many of the most highly expressed genes in dormant states were stress-related even in the absence of abiotic stress, indicating that ABA, stress and dormancy responses overlap significantly at the transcriptome level.