This review focuses on the biochemical and physiological response of the halotolerant green alga, Dunaliella salina, to conditions of stress. It is now well established that in response to stress, cells of Dunaliella salina var. bardawil show increased glycerol production, massive βcarotene accumulation and enhanced abscisic acid metabolism. In this respect, cellular responses are regulatory and seem to depend on a diversity of mechanisms which may be linked to a modification of the abscisic acid balance. Dunaliella lacks a rigid cell wall and the cellular contents are enclosed by an elastic plasma membrane that permits rapid cell volume changes in response to extracellular changes in osmolarity. Based on the ‘stretch activated ion channels model’ reviewed recently by Kirst (1990) we propose the following cascade of responses: volume change/distortion of plasmalemma→change in pH→redistribution of abscisic acid→inhibition of H⁺-ATPase→[increased abscisic acid levels]→opening of Ca²⁺ channels→influx of Ca²⁺→rise in cytosolic Ca²⁺→[→increased abscisic acid levels]→effect on metabolism (activity of enzymes).

The interrelationship between abscisic acid (ABA) production and β-carotene accumulation was investigated in salt-stressed cells of the halotolerant green alga Dunaliella salina var bardawil. Cells were supplied with either R-[2-¹⁴C]mevalonolactone or [¹⁴C] sodium bicarbonate for 20 hours and then exposed to increased salinity (1.5 to 3.0 molar NaCl) for various lengths of time. Incorporation of label into abscisic acid and phaseic acid and the distribution of [¹⁴C]ABA between the cells and incubation media were monitored. [¹⁴C]ABA and [¹⁴C]phaseic acid were identified as products of both R-[2-¹⁴C]mevalonolactone and [¹⁴C]sodium bicarbonate metabolism. ABA metabolism was enhanced by hypersalinity stress. Actinomycin D, chloramphenicol, and cycloheximide abolished the stress-induced production of ABA, suggesting a role for gene activation in the process. Kinetic analysis of both ABA and β-carotene production demonstrated two stages of accelerated β-carotene production. In addition, ABA levels increased rapidly, and this increase occurred coincident with the early period of accelerated β-carotene production. A possible role for ABA as a regulator of carotenogenesis in cells of D. salina is therefore discussed.