Induced plant defences are those defences which are initiated after a pathogen infection has been detected. These defences are chemical changes within the cell wall which cause the formation of papillae, which in fungal attack form reinforced areas around the penetration peg, preventing the full insertion of the peg, Buchanan et al. (2000). The papillae are formed from callose and lignin. The lignification of the cell wall and callose deposition in the plasmodesmata give improved physical strength to prevent pathogen penetration, prevent pathogenic toxin diffusion and also prevent solute leakage from the plant cells, therefore starving the pathogens of nutrition. Wound responses, from insect herbivores are triggered by the plant hormones jasmonic acid (JA) and ethylene. These hormones take part in the signalling pathway which leads to the production and release of reactive oxygen species (ROAs) such as H2O2 and polyphenol oxidase (PPOs), the ROAs are directly toxic to microbial pathogens which may enter the wound while the PPOs prevent the herbivore from digesting any plant material such as leaf fibre and solutes from being digested in the gut, thus rendering the plant material useless as a food source. The hypersensitive response (HR) is also a mechanism which seems to be controlled by the plant in which a pathogen initiates the rapid cell death of the infected cell and the surrounding cells. This seems to prevent the pathogen from spreading and infecting the rest of the plant and allowing the plant to repair without the risk of further infection.
Water deficit under drought conditions in plants is combated foremost by stomatal inhibition. This involves the closure of the stomata when water levels are low and transpiration rates are high and is controlled by asbisic acid or ABA. Under water deficit, total plant growth is also effected directly, being reduced.
In plants, the stomata or guard cells which act as gas exchange pores are closed when the cells are flaccid and are open as turgor increases. ABA mediates the response of stomata hydroactively closing in response to water deficit. ABA binds to receptor R, which results in an increase in free cytosolic Ca2+ through Ca2+ release from internal cellular stores or via Ca2+ influx from extracellular sources. The increase of Ca2+ inhibits the opening of K+IN channels and promotes the opening of K+OUT and anion channels in the plasma membrane. Due to the reduction of these ions in the cell, there is also a reduction of water in the cell, which in turn causes a loss of turgor and so the stomatal pore becomes flaccid and closes. When the stomata are closed, transpiration is reduced and therefore the amount of water being lost is at a minimum.
Salt stress is defined as “Stress caused by concentrations of salt greater than that required for optimum growth of a typical crop plant (1500ppm or 25mM Na+)” The main stresses imposed which the plants must respond to are water deficits and a shift in the ion concentrations in the vacuoles of the cells.
Plants have evolved to combat salt stress on three levels. Firstly, there are halophytes, plants which are tolerant to salt but do not grow in highly saline conditions. There are then glycophytes, which can tolerate salt, but not to the extent of halophytes. Finally there are euhalophytes, or true halophytes. These plants are able to tolerate high salt levels and are even stimulated to grow in environments which show a high salinity. In response to the effects of increased salinity, strategies include a fine regulation and rate of movement through the plant of NaCl , the adjustment of osmotic potentials via the compartmentalisation of ions in the cells. The regulation of NaCl uptake and movement is achieved by the selective uptake of NaCl and the movement of the salts into the xylem. As the salts move up through the xylem, they are moved into “salt glands” via the phloem and then from these glands, the salt is excreted. To achieve an osmotic adjustment, Na+ and Cl- ions need to be compartmentalised in the vacuole and this occurs via a series of proton driven ion channels. Because of the increase of these ions in the vacuole, osmosis occurs, pulling more water up through the xylem and into the cells, and so water deficits are reduced.
Plants respond to both high and low temperatures. Under high temperatures, universal and highly conserved heat-shock proteins (HSPs) are synthesised. These give an increased tolerance and recovery rate to high temperatures by either acting as molecular chaperones, protecting proteins from heat damage or by aiding in the degradation of proteins which have already suffered heat damage. Under low temperatures, there is an increase in unsaturated fatty acids in chloroplast membrane lipids which provide insulation and allow photosynthesis to occur up to a certain point. Plants also synthesise anti-freeze proteins which specifically bind to ice crystals and prevent them from growing. By limiting the crystal sizes, the amount of damage to the plants structure is limited.
In conclusion, plants have to endure many environmental stresses. To combat these they have developed many diverse and unique responses.
References
Evidence for an Extracellular Reception Site for Abscisic Acid in Commelina Guard Cells, B. E. Anderson, J. M. Ward and J. I. Schroeder Plant Physiology , 104, Issue 4 1177-
How can Stomata Contribute to Salt Tolerance? (1997) M. F. Robinson, A. Vếry, D. Sanders and T.A. Mansfield Annals Of Botany, 80; 387-393
Plant Responses to Water Stress (1973), T. C. Hsiao, Annual Review of Plant Physiology 24
Biochemistry and Molecular Biology Of Plants (2000) B.B Buchanan, W. Gruissem and R. L. Jones
Lecture Notes: Biol 341Salt Stress, Dr Martin McAnish, Biol 341How Do Plants Grow And Function During Water Deficit? Dr M Bacon