Abstract

Plant cells respond to short-term stress dehydration by modification of internal Ψ π such that an inward gradient of Ψ ω is maintained. In response to lowered Ψ ω, increases in internal Ψ π are created by alteration of cell inorganic ions and small organic solute content. Passive movement of water follows, changing cell hydration and forcing the plasma membrane against the elastic cell wall. The stretched cell wall presses against the cell contents, creating a hydrostatic pressure, Ψ π, which tends to force water out of the cell. The resulting hydrostatic pressure eventually comes into equilibrium with forces bringing water into the cell, largely Ψ π, and the net flow of water ceases. The mechanism for sensing cell Ψ ω changes is unknown but the initial event must be physical, not biochemical. The method of translation of such physical events into biochemical actions is also unknown but the Zimmermann model provides a means of signal transduction and amplification, through the alteration of membrane parameters, which could account for the observed changes. As for animal cells, cell levels of Ca 2+ are important for their regulation of membrane P j in these responses but unlike osmoregulation in higher animals, the involvement of plant hormones in these responses have not been clearly established. However, the important role of plant cell limiting membranes in plant cell osmoregulation responses seems obvious.

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