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Plant Physiology Laboratory, The Lowdermilk Faculty of Agricultural Engineering, Technion-Israel institute of Technology, Haifa 32,000, Israel
* Corresponding author (agpetern{at}techunix.technion.ac.il).
Reductions in rates of cell and tissue growth are a commonly observed response to water deficits resulting from drought or soil salinity. These can lead to reductions in plant size and yields. More severe stress can lead to accelerated death and complete loss of yields. This review deals with the final biophysical links in the chain of events underlying inhibition of growth in crop plants exposed to water deficits. It first examines and rejects the notion that a stress-induced reduction in cellular turgor pressure is necessarily a primary cause of growth inhibition. Data supporting the involvement of an additional and often overlooked biophysical response to water deficits are then reviewed: This response involves changes in tissue extension capacity, as a result of hardening (or softening) of expanding cell walls, and is termed cell wall adjustment. Wall hardening should increase the capacity of expanding cells to maintain turgor pressure but also acts to inhibit rates of cell expansion growth. The inhibition of cell expansion can lead to reductions in leaf area that limit rates of transpirational loss of soil water reserves; in nonirrigated crops exposed to terminal drought environments, this adaptation may prolong survival and allow time for completion of reproductive development. Conversely, wall hardening responses to intermittent water deficit episodes, e.g., in irrigated crops, could be undesirable. The survival of irrigated crops is largely assured and induction of wall hardening in the intervals between irrigation could unnecessarily reduce growth and yields. Appropriate manipulation of cell wall adjustments, via selection, breeding, or genetic engineering, could prove useful for the development of more stress-resistant crop plants suited to irrigated or nonirrigated environments.
Received for publication November 8, 1994.
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