Early steps in cold sensing by plant cells: the role of actin cytoskeleton and membrane fluidity
Article first published online: 25 DEC 2001
The Plant Journal
Volume 23, Issue 6, pages 785–794, September 2000
How to Cite
Örvar, B. L., Sangwan, V., Omann, F. and Dhindsa, R. S. (2000), Early steps in cold sensing by plant cells: the role of actin cytoskeleton and membrane fluidity. The Plant Journal, 23: 785–794. doi: 10.1046/j.1365-313x.2000.00845.x
- Issue published online: 25 DEC 2001
- Article first published online: 25 DEC 2001
- Received 5 May 2000;revised 23 June 2000;accepted 30 June 2000.
- cold acclimatization;
- membrane fluidity
Many plants acquire freezing tolerance through cold acclimatization (CA), a prolonged exposure to low but non-freezing temperatures at the onset of winter. CA is associated with gene expression that requires transient calcium influx into the cytosol. Alfalfa (Medicago sativa) cells treated with agents blocking this influx are unable to cold-acclimatize. Conversely, chemical agents causing increased calcium influx induce cold acclimatization-specific (cas) gene expression in alfalfa at 25°C. How low temperature triggers calcium influx is, however, unknown. We report here that induction of a CA-specific gene (cas30), calcium influx and freezing tolerance at 4°C are all prevented by cell membrane fluidization, but, conversely, are induced at 25°C by membrane rigidification. cas30 expression and calcium influx at 4°C are also prevented by jasplakinolide (JK), an actin microfilament stabilizer, but induced at 25°C by the actin microfilament destabilizer cytochalasin D (CD). JK blocked the membrane rigidifier-induced, but not the calcium channel agonist-induced cas30 expression at 25°C. These findings indicate that cytoskeleton re-organization is an integral component in low-temperature signal transduction in alfalfa cell suspension cultures, serving as a link between membrane rigidification and calcium influx in CA.