Induction of desiccation tolerance in plant somatic embryos: how exclusive is the protective role of sugars?

Abstract

Plant somatic embryos usually lack desiccation tolerance. They may acquire such a tolerance upon preculture in the presence of abscisic acid (ABA), followed by slow drying, but not fast drying. ABA causes torpedo-shaped somatic embryos to lose their chlorophyll, suspend growth, exhibit low rates of respiration, and maintain elevated sucrose contents. The subsequent slow drying leads to a partial conversion of sucrose into oligosaccharides and the expression of dehydrin transcripts. Slow-dried, desiccation-tolerant somatic embryos have stable membranes, retain their native protein secondary structure, and have a densely packed cytoplasmic glassy matrix. Fast-dried, desiccation-sensitive somatic embryos experience some loss of phospholipids and an increase in free fatty acids. Their proteins show signs of denaturation and aggregation, and the glassy matrix has reduced hydrogen bonding. The reduced conversion of sucrose into oligosaccharides appears not to underlie dehydration injury. Proteins in slow-dried somatic embryos, not pretreated with ABA, also show signs of denaturation, which might be attributed to low sugar contents. We conclude that by reducing cellular metabolism, ABA maintains high sugar contents. These sugars contribute to the stability of membranes, proteins, and the cytoplasmic glassy matrix, whereas slow drying permits a further fine tuning of this stability. Partitioning of endogenous amphiphiles from the cytoplasm into membranes during drying may cause membrane perturbance, although it might confer protection to membranes in the case of amphiphilic antioxidants. The perturbance appears to be effectively controlled in desiccation-tolerant systems but not in sensitive systems, for which we suggest dehydrins are responsible. In this context, the low desiccation tolerance in the presence of ample sugars is discussed.