Recently, Professor Huang Wei's team at the College of Life Sciences, South China Agricultural University, discovered a new pathway in Arabidopsis thaliana's circadian clock core oscillator that regulates abscisic acid and cold stress signals. The findings were published in "Plant, Cell & Environment."
The anticipatory regulatory mechanism evolved by organisms to adapt to their environment, known as the circadian clock, is crucial for plants to respond to environmental stresses. With the intensification of global climate change leading to an increase in the frequency of freezing disasters, severely affecting crop productivity and stability, research on the mechanisms of plant responses to cold stress induced by day-night environmental changes remains limited.
This study revealed that the Arabidopsis circadian clock core oscillator TOC1 (a key nighttime gene in the circadian clock) regulates the abscisic acid signaling pathway and cold stress response by inhibiting the MYB44 gene. Through bioinformatics analysis of RNA-Seq and ChIP-Seq data of the Arabidopsis circadian clock gene TOC1, the team identified the direct downstream gene MYB44, confirming its rhythmicity and regulation by TOC1. The research also found that TOC1 and MYB44 can respond to cold stress through both abscisic acid-dependent and abscisic acid-independent mechanisms to ensure appropriate responses to various stresses, maintaining a balance between normal physiological processes and stress responses that consume energy.
This study is the first to discover that the Arabidopsis circadian clock core oscillator TOC1 is closely involved in the regulation pathway upstream of abscisic acid. By revealing the regulatory pathways of the Arabidopsis circadian clock in response to abscisic acid signals and cold stress, it provides new insights for breeding high-quality cold-resistant crops and offers a deeper understanding of the regulatory network connecting the circadian clock, abscisic acid signaling, and stress response genes.
Link to the research paper: https://doi.org/10.1111/pce.14922
Simplified model of TOC1 regulating MYB44 in ABA signaling and cold stress. Research team provided the figure.
(Note: This simplified model illustrates the regulatory role of the TOC1-MYB44 module in ABA signaling and its response to cold stress. ABA treatment dose-dependently induces TOC1 expression. Interestingly, cold stress independently of ABA presence triggers rapid induction of TOC1. Furthermore, TOC1 rhythmically inhibits MYB44 expression, demonstrating negative regulation of ABA signaling and cold stress response. Bold arrows indicate faster, easier induction.)
