Cold (chilling) tolerance genes Which gene has been shown to enhance chilling resistance by maintaining membrane function at low temperatures?

Introduction / Context:
Chilling injury arises when membranes lose fluidity at low temperatures, causing leakage and metabolic disruption. Genetic strategies to increase unsaturated fatty acids in membranes can improve plant performance under chilling.

Given Data / Assumptions:

• Membrane lipid composition strongly influences low-temperature fluidity.
• Acyltransferases involved in glycerolipid biosynthesis can shift saturation profiles.
• Other listed genes perform unrelated functions (cell wall softening, ethylene metabolism, carbohydrate partitioning).

Concept / Approach:
Overexpression of certain glycerolipid pathway enzymes (e.g., glycerol-3/1-phosphate acyltransferase from chilling-tolerant species) can increase unsaturation in thylakoid and plasma membranes, stabilizing photosynthesis and ion balance during cold stress.

Step-by-Step Solution:

Verification / Alternative check:
Studies in tobacco and Arabidopsis showed that introducing acyltransferase genes from chilling-tolerant plants improved photosystem function and survival at low temperature.

Why Other Options Are Wrong:

• Polygalacturonase: fruit softening, not cold tolerance.
• ACC deaminase: affects ethylene levels and stress signaling but is not the classic chilling-tolerance structural gene.
• Sucrose phosphate synthase: influences sucrose synthesis; may aid stress indirectly, but not the canonical membrane-stabilizing mechanism.
• Dihydrofolate reductase: unrelated to cold membranes.

Common Pitfalls:
Assuming general stress-related enzymes equal targeted membrane modifications needed for chilling tolerance.

Final Answer:
Glycerol-1-phosphate acyltransferase