These authors contributed equally to this work.
Involvement of the abscisic acid catabolic gene CYP707A2 in the glucose-induced delay in seed germination and post-germination growth of Arabidopsis
Version of Record online: 4 OCT 2011
Copyright © Physiologia Plantarum 2011
Volume 143, Issue 4, pages 375–384, December 2011
How to Cite
Zhu, G., Liu, Y., Ye, N., Liu, R. and Zhang, J. (2011), Involvement of the abscisic acid catabolic gene CYP707A2 in the glucose-induced delay in seed germination and post-germination growth of Arabidopsis. Physiologia Plantarum, 143: 375–384. doi: 10.1111/j.1399-3054.2011.01510.x
- Issue online: 3 NOV 2011
- Version of Record online: 4 OCT 2011
- Accepted manuscript online: 24 AUG 2011 08:17AM EST
- Received 7 April 2011; revised 23 May 2011
Earlier studies showed that sugars as signaling molecules play pivotal roles in the regulation of seed germination. ABA biosynthesis upregulation is suggested as one of the possible mechanisms mediating the glucose-induced delay in seed germination. In this study, the role of ABA catabolism in glucose-induced inhibition was investigated. Using Arabidopsis thaliana seeds, the results show that the repression of ABA catabolism by diniconazole aggravated the glucose-induced delay in seed germination. The transcript and protein profiles of CYP707A2, a key gene encoding ABA 8′-hydroxylase in ABA catabolism in Arabidopsis, were significantly decreased by exogenous glucose treatment. Transgenic experiments confirmed that the over-expression of the CYP707A2 gene alleviated the glucose-induced inhibition effect, whereas the cyp707a2 mutant seeds displayed a hypersensitivity to glucose during imbibition. Exogenous glucose also arrested the early seedling development of Arabidopsis. The CYP707A2 over-expression seedlings exhibited lower ABA levels and seemed less sensitive to exogenous glucose compared with wild type seedlings. In summary, the glucose-induced delay in seed germination and seedling development is directly related to the suppression of ABA catabolism through the repression of the CYP707A2 expression.