Early steps in cold sensing by plant cells: the role of actin cytoskeleton and membrane fluidity

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<jats:title>Summary</jats:title><jats:p>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 (<jats:italic>Medicago sativa</jats:italic>) cells treated with agents blocking this influx are unable to cold‐acclimatize. Conversely, chemical agents causing increased calcium influx induce cold acclimatization‐specific (<jats:italic>cas</jats:italic>) 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 (<jats:italic>cas30</jats:italic>), 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. <jats:italic>cas30</jats:italic> 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 <jats:italic>cas30</jats:italic> 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.</jats:p>

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