Opening And Closing Of Stoma-Bn
7.1 Drought and salinity #
7.1.1 Stomata, compatible solutes, and LEA proteins #
Drought lowers water potential. The fast response is stomatal closure (Chapter 1), which saves water and cuts CO2, so photorespiration and ROS rise if light continues. Osmotic adjustment accumulates solutes so that ฮจs falls and some turgor remains. The vacuole can use K+. The cytosol uses compatible solutes โ proline, glycine betaine, sugars, mannitol, pinitol โ which do not poison enzymes and which stabilise proteins and membranes. LEA proteins, including dehydrins, are disordered proteins induced by drought, cold, and ABA. They accompany desiccation tolerance. No single folding mechanism should be memorised.
Shape changes are slower still: rolled maize leaves, smaller leaves, more cuticle, loss of old leaves, a higher root:shoot ratio. Craterostigma can dry its leaves and recover. Ordinary crops cannot. Their tolerant stage is the seed.
7.1.2 Exclusion and the vacuole #
Salinity injures in two ways that do not arrive together. The osmotic injury is immediate: soil ฮจ falls and the shoot behaves as in drought. The ionic injury develops as Na+, and often Clโ, accumulate in the leaves that have transpired longest, so old leaves burn first. Na+ competes with K+. Most crops are glycophytes. Halophytes such as Salicornia and Atriplex use vacuolar Na+ as a cheap osmoticum. Exclusion without osmotic adjustment cannot extract water, and cytosolic Na+ poisons the cell.
In Arabidopsis a salt-induced calcium signal activates SOS3 (CBL4) and the kinase SOS2 (CIPK24), which switches on SOS1, a plasma-membrane Na+/H+ antiporter. HKT1 retrieves Na+ from the xylem. Tonoplast NHX exchangers, driven by the vacuolar proton pumps, park Na+ in the vacuole. Compatible solutes in the cytosol balance that vacuolar osmolarity. Salt adds a toxic ion. It does not invent a new kind of water potential.
7.2 Temperature and oxygen #
7.2.1 Heat, chilling, and freezing #
Heat fluidises membranes and unfolds proteins. PSII and Rubisco activase fail early. Heat-shock proteins limit the damage: small HSPs bind unfolded chains, HSP70 and HSP90 refold clients, and HSP100 can disentangle aggregates. Heat-shock factors are released when unfolded proteins occupy the chaperones that had been holding the factors inactive. A sublethal heat improves survival of a later severe heat. That acquired thermotolerance is not the same as being native to a hot climate. Open stomata can cool a leaf if the soil can pay. If it cannot, the leaf closes and heats further.
Chilling injury is damage above 0ยฐC, often below about 10โ12ยฐC, in banana, rice, maize, tomato, cucumber, and cotton. Membranes that are too saturated become rigid, proteins stop working, and the tissue leaks, often after the return to warmth. Tolerant plants put more double bonds into their fatty acids and stay fluid. Freezing is different. Ice usually forms first in the apoplast and pulls water out of the cells. Survival is survival of that dehydration. Intracellular ice is generally lethal. Days of low, non-freezing temperature acclimate winter rye, winter wheat, and Arabidopsis: CBF/DREB1 factors induce COR genes, including LEA proteins, and sugars accumulate. Chilling is a rigid membrane. Freezing is ice.
7.2.2 Aerenchyma and fermentation #
O2 diffuses about 10,000 times more slowly in water than in air, so a waterlogged soil goes hypoxic and then anoxic. Ethylene accumulates, and reduced Fe2+, Mn2+, and sulphide add a chemical toxicity. Roots lose hydraulic conductivity, partly because an acidic cytosol closes aquaporins, and the shoot can wilt in mud. Tomato petioles bend down, an epinastic ethylene and auxin response.
Aerenchyma is a gas path through the cortex. In maize and rice it forms by ethylene-promoted death of cortical cells, with ROS in the signal. Some species separate cells without killing them. Rice also limits radial O2 leakage so that what enters reaches the tip. Without O2, ATP falls to the 2 ATP of glycolysis, against an aerobic yield of the order of 30. Lactate dehydrogenase regenerates NAD+ and acidifies the cell, usually briefly. Alcohol dehydrogenase makes ethanol, which can diffuse away, and also regenerates NAD+. Glycolysis speeds up and reserves disappear.
Rice uses that trapped ethylene in opposite ways. SUB1A restrains elongation in a short deep flood and saves carbohydrate. SNORKEL genes elongate deepwater-rice internodes so that leaves stay above a rising flood.
7.3 ROS and biotic stress #
7.3.1 Scavenging, in principle #
Reactive oxygen species rise when electron transport is over-reduced: bright light with shut stomata, chilling, salinity, and the Mehler reaction, in which PSI reduces O2 to superoxide. Singlet oxygen comes from triplet chlorophyll. Hydrogen peroxide comes from superoxide dismutase and from glycolate oxidase. The hydroxyl radical, formed when peroxide meets free iron or copper, is not scavenged by any useful enzyme. The defence is to keep those reactants apart. ROS damage lipids, proteins, and DNA. At a lower dose, and in a defined place, H2O2 is also a signal, in guard cells, aerenchyma, and defence.
Superoxide dismutase converts superoxide to peroxide. Catalase, in the peroxisome, clears the photorespiratory flux without spending a reductant. Chloroplasts lack catalase and use ascorbate peroxidase. In the ascorbateโglutathione cycle, ascorbate reduces peroxide, glutathione reduces dehydroascorbate, and NADPH regenerates glutathione. Tocopherol and carotenoids quench singlet oxygen in membranes. Low lumen pH also converts violaxanthin to zeaxanthin, and zeaxanthin with PsbS dumps excess light as heat. The gradient that makes ATP is also a safety valve.
7.3.2 Gene-for-gene resistance #
Flor’s gene-for-gene result on flax and flax rust is the genetic statement: a host resistance gene matches a pathogen avirulence gene, and disease proceeds if either is missing. Pathogens deliver effectors that suppress a broader immunity, in which membrane receptors detect molecules such as flagellin or chitin. Many R genes encode NLR proteins that recognise an effector or the damage it does to a host protein. Recognition triggers a hypersensitive response: local cell death, ROS, callose, and phytoalexins. That contains a biotroph, which needs living cells, and is a poor answer to a necrotroph, which is more often limited by jasmonate. Distant leaves can then become primed. Systemic acquired resistance requires salicylic acid and NPR1, as Chapter 5 said, and the travelling signal is the unsettled part. This is not the antibody system of Immunology.
7.4 Key terms, summary, and self-check #
Key terms. Compatible solute; LEA; SOS1; NHX; chilling; CBF; aerenchyma; fermentation; ascorbateโglutathione cycle; hypersensitive response; systemic acquired resistance.
Summary. Drought closes stomata and later accumulates compatible solutes and LEA proteins. Salinity adds Na+ toxicity to an osmotic drought; SOS1 extrudes Na+ and NHX stores it in the vacuole. Heat is met with chaperones, chilling with unsaturated membranes, and freezing with CBF-dependent acclimation to extracellular ice. Flooding is met with aerenchyma and fermentation, and rice uses ethylene either to wait or to elongate. ROS are scavenged by SOD, catalase, and the ascorbateโglutathione cycle. Specific disease resistance is gene-for-gene recognition, a local hypersensitive response, and salicylic-acid-dependent priming of the rest of the plant.
Self-check.
1. Why is proline a compatible solute, while the same osmolarity of cytosolic Na+ is not a remedy for drought?
2. Which part of salinity injury is immediate, which part develops in old leaves, and which tonoplast exchanger sequesters Na+?
3. Why are banana and rice injured by temperatures that form no ice, and what does a cold, non-freezing week change in winter rye?
4. What is aerenchyma for, and why does hypoxia push pyruvate toward ethanol or lactate?
5. State the gene-for-gene idea, and say why a hypersensitive response suits a biotroph better than a necrotroph.
