As organisms that cannot move, plants have evolved precise response mechanisms to various environmental stresses, including drought, low temperature, disease, and mechanical damage.
Basic Knowledge
Drought-stress response: ①ABA (abscisic acid) acts on the guard cells of leaves → K⁺ and Cl⁻ flow out → the cell’s osmotic pressure decreases → water flows out → stomatal closure. ② Compatible solutes such as osmotin and proline accumulate in cells → osmotic adjustment. ③ Dehydration-stress proteins (such as LEA proteins) protect cells.
Low-temperature stress (cold acclimation): ①Increase in unsaturated fatty acids → maintenance of membrane fluidity (prevention of membrane hardening). ② Antifreeze proteins and ice-nucleating proteins. ③ Accumulation of anthocyanins and sugars → lowering of the freezing point and antioxidation.
Disease and herbivore resistance: ①Salicylic acid (SA) = accumulates after pathogen infection → induces systemic acquired resistance (SAR) and synthesis of PR (pathogenesis-related) proteins. ②Jasmonic acid (JA) = increases after mechanical damage or insect feeding → synthesis of protease-inhibitor proteins and toxins → inhibition of insect digestive enzymes. ③Volatile organic compounds (VOCs) = released by wounded plants, allowing neighboring plants to receive an “alarm” and strengthen resistance in advance.
Photooxidative stress and reactive oxygen species (ROS): Excess ROS (H₂O₂, OH·, and O₂⁻) are produced by strong light and UV → lipid peroxidation, protein denaturation, and DNA damage. Defense: antioxidant mechanisms involving SOD (superoxide dismutase), catalase, ascorbic acid, tocopherol, and others.
Plant immunity (PTI and ETI): ① PAMP-triggered immunity (PTI): pattern-recognition receptors recognize pathogen-derived components (PAMPs) → defense responses. ② Effector-triggered immunity (ETI): products of R genes recognize pathogen effectors → hypersensitive cell death (HR) prevents the spread of infection.
Explain how plants exhibit systemic acquired resistance (SAR), including the role of salicylic acid.
Answer: Salicylic acid (SA) is produced and accumulates in a local leaf infected by a pathogen. SA is transported throughout the plant through the phloem (or its precursor MeSA is transmitted as a gas), inducing transcription of defense genes (such as PR genes) in uninfected leaves. As a result, leaves throughout the plant acquire resistance to the pathogen. This phenomenon is called SAR and can be described as a plant “immune memory” similar to vaccination.
- Drought → ABA → stomatal closure (K⁺ outflow from guard cells)
- Cold acclimation = increased unsaturated fatty acids, sugar accumulation, and antifreeze proteins
- Salicylic acid = pathogen resistance and systemic acquired resistance (SAR)
- Jasmonic acid = insect-feeding response and induction of protease inhibitors
- VOCs = volatile substances that warn neighboring plants
- ROS removal = SOD, catalase, and ascorbic acid
- Hypersensitive cell death (HR) = infected cells kill themselves to prevent spread of the pathogen
Points to Note
① ABA is a major signal molecule for drought stress, and stomatal closure also limits CO₂ uptake for photosynthesis, creating a trade-off with water-use efficiency. ② Systemic acquired resistance (SAR) is inducible defense and resembles the “priming” of innate immunity in animals in that the entire plant is strengthened after the initial infection. ③ Jasmonic-acid and salicylic-acid signals may act antagonistically, and plants switch signals according to the type of pathogen.
Practice
- Explain the mechanism by which ABA acts on guard cells to close stomata during drought stress, based on ion movement and changes in osmotic pressure.
- Explain the defensive action of jasmonic acid synthesized when a plant is damaged by insect feeding.
- Name two enzymes that mainly function in the removal of reactive oxygen species (ROS) in plants.