A3 Thermal Stress (heat and frost)

Topic

The leaf-atmosphere interface is the contact surface between the leaf and the surrounding air; it determines the leaf temperature reached by the leaf tissue at any given moment. This interface regulates the exchange of heat and water vapor between the leaf and the air, and this exchange dictates the tissue's actual leaf temperature.

Thermal stress occurs when the leaf temperature moves outside the leaf's optimal enzymatic range—a shift that can happen in two opposite directions: an excess, when the leaf temperature rises too high, or a deficit, when it drops too low. Each of these directions subsequently triggers a different damage mechanism within the leaf tissue.

When the leaf temperature rises above a range of approximately 40 to 45 degrees Celsius, Rubisco and the thylakoid membranes within the leaf tissue become denatured; the excessive leaf temperature causes this protein and these membranes to lose their functional structure, thereby disrupting the leaf's enzymatic activity.

Conversely, when the leaf temperature drops below zero degrees Celsius, freezing occurs, causing water to crystallize first in the leaf tissue's apoplast; if the temperature continues to fall, crystallization progresses until it reaches the interior of the leaf cells.

The leaf-atmosphere interface is also the site where the leaf's adaptive responses to these two types of thermal stress take place. In response to excessive leaf temperature, the leaf opens its stomata to cool down; this opening increases water vapor exchange at the leaf-atmosphere interface, and the resulting increase in exchange lowers the leaf temperature, closing the loop between the leaf's response and the temperature that triggered it. In response to excessive leaf temperature, the leaf synthesizes heat-shock proteins that protect Rubisco and thylakoid membranes from denaturation without altering the leaf temperature itself. Conversely, in response to low leaf temperature, the leaf synthesizes cryoprotectants—such as sucrose, proline, and LEA proteins—that protect the apoplast and cells from water crystallization, again without modifying leaf temperature.

Ultimately, the thermal stress experienced by the leaf is resolved differently depending on the direction in which the leaf temperature has deviated from the optimal enzymatic range: if stomatal opening successfully lowers the leaf temperature in time, or if heat-shock proteins protect Rubisco and thylakoid membranes, the leaf avoids irreversible denaturation; if cryoprotectants successfully protect the apoplast and cells, the leaf avoids irreversible damage caused by water crystallization; however, if the leaf temperature remains outside the optimal enzymatic range for too long without these adaptive responses taking effect at the leaf-atmosphere interface, the thermal stress results in irreversible damage to the leaf tissue.

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