A role for multiple circadian clock genes in the response to signals that break seed dormancy in Arabidopsis

Steven Penfield, Anthony Hall, Karen Halliday (Group Leader)

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Plant seeds can sense diverse environmental signals and integrate the information to regulate developmental responses, such as dormancy and germination. The circadian clock confers a growth advantage on plants and uses environmental information for entrainment. Here, we show that normal circadian clock gene function is essential for the response to dormancy-breaking signals in seeds. We show that mutations in the clock genes LATE ELONGATED HYPOCOTYL, CIRCADIAN CLOCK ASSOCIATED1 (CCA1), and GIGANTEA (GI) cause germination defects in response to low temperature, alternating temperatures, and dry after-ripening. We demonstrate that the transcriptional clock is arrested in an evening-like state in dry seeds but rapidly entrains to light/dark cycles in ambient temperatures upon imbibition. Consistent with a role for clock genes in seed dormancy control, CCA1 expression is transcriptionally induced in response to dry after-ripening and that after-ripening affects the amplitude of subsequent transcriptional clock gene oscillations. Control of abscisic acid- and gibberellin-related gene expression in seeds requires normal circadian function, and GI and TIMING OF CAB EXPRESSION1 regulate the response to ABA and GA in seeds. We conclude that circadian clock genes play a key role in the integration of environmental signaling controlling dormancy release in plants.
Original languageEnglish
Pages (from-to)1722-1732
Number of pages11
JournalPlant Cell
Issue number6
Publication statusPublished - Jun 2009

Keywords / Materials (for Non-textual outputs)

  • Abscisic Acid
  • Arabidopsis
  • Arabidopsis Proteins
  • Circadian Rhythm
  • Gibberellins
  • Molecular Sequence Data
  • Mutation
  • Phenotype
  • Plant Growth Regulators
  • RNA, Messenger
  • Seeds
  • Signal Transduction
  • Transcription Factors


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