Karen L. Koster, Ph.D.
Research Interests

Department of Biology
The University of South Dakota
414 E. Clark Street
Vermillion, SD 57069
Phone: 1-605-677-6173
Fax: 1-605-677-6557
E-mail: Karen.Koster@usd.edu

Research Interests

When mature, many angiosperm seeds can survive the loss of greater than 80% of their cellular water with little or no damage to their membranes. Once the seeds begin to germinate, however, tolerance of dehydration is progressively lost. This provides a convenient system that can be exploited for the study of desiccation tolerance. Previous students in my lab have characterized the loss of desiccation tolerance in pea embryos during germination to provide a framework for our research [14]. With this framework in place, my students and I can explore various aspects of seed physiology, biophysics, biochemistry, and ultrastructure to try to unravel the mechanisms that confer desiccation tolerance to the embryo.

Before mechanisms of desiccation tolerance can be completely understood, however, it is first necessary to understand how water loss damages cells that are sensitive to this stress. Dehydration of sensitive cells disrupts many metabolic systems [21], but it is generally considered that cell membranes are a primary site of desiccation damage [5,11,17], and that preventing damage to membranes is of key importance in desiccation tolerance. Most of my research efforts have been directed to understanding how membranes are affected by dehydration, and how they might be protected from damage by cellular components, such as sugars. My students and I have studied desiccation tolerance and membrane behavior in whole organisms [14], isolated cells [8,20], and model membranes [5,7,9-10].

Many studies of the role of membranes in desiccation tolerance have compared membranes in desiccated systems to membranes in fully hydrated systems, but have not observed the events that occur during the process of dehydration. Students in my lab have developed techniques for isolating protoplasts from desiccation tolerant embryos [8,16,20], and we have been using these protoplasts to more directly observe how the plasma membrane behaves during dehydration [2,3,12,13,15]. We have determined that there are important differences between the tolerance of the isolated protoplasts and the tolerance of the tissue from which they were isolated [20], and we are exploring these differences to further understand how various factors, such as the presence of different solutes, affect membrane integrity. Plasma membrane behavior during freeze-induced dehydration is known to be crucial for freezing tolerance in leaf tissues [18,19], and we are finding that similar behaviors may be important in dehydrating embryos [2].

Much of my previous and current work has focused on the role of soluble sugars in desiccation tolerance [4-7,9,10]. It is widely accepted that non-reducing sugars are an important component of desiccation tolerance in seed embryos and in other organisms. Sugars are known to protect cellular membranes from the deleterious effects of dehydration; my students and I have been using biophysical techniques, primarily differential scanning calorimetry (DSC), to study the effects of sugars and other solutes on the phase behavior of lipids at various levels of dehydration. We have demonstrated that sugars can stabilize membranes by physically hindering the close approach of membranes and other hydrophilic surfaces, thereby limiting the hydration forces that can otherwise compress membrane components and cause phase changes in the lipids [1,5,7]. We were also the first to show that glass formation by sugar solutions can have profound effects on the membranes [5,7,10], and presumably this physical effect extends to other macromolecules in the dehydrated cells. Many questions remain about the specificity of solute effects on membrane phase behavior, and we are continuing this work, using DSC and other techniques to measure the fundamental physical properties of membranes, solutions and macromolecules at a range of water contents.

1. Bryant G, Koster KL, Wolfe J (2001) Membrane behaviour in seeds and other systems at low water content: the various effects of solutes. Seed Science Research 11: 17-25.

2. Halperin SJ, Koster KL (2005) Desiccation tolerance of protoplasts from Pisum sativum enhanced by sucrose uptake. Presented at the 8th International Workshop on Seeds, Brisbane, Australia.

3. Halperin SJ, Rowen R, Koster KL (2004) Desiccation damage and tolerance in pea embryo protoplasts related to oxidative stress and sugar content. Presented at Plant Biology 2004, the Annual Meeting of the American Society of Plant Biologists, Orlando, FL. Abstract # 991.

4. Koster KL (1991) Glass formation and desiccation tolerance in seeds. Plant Physiology 96: 302-304

5. Koster KL, Lei YP, Anderson M, Martin S, Bryant G (2000) Effects of vitrified and non-vitrified sugars on phosphatidylcholine fluid-to-gel phase transitions. Biophysical Journal 78: 1932-1946

6. Koster KL, Leopold AC (1988) Sugars and desiccation tolerance in seeds. Plant Physiology 88: 829-832

7. Koster KL, Maddocks KJ, Bryant G (2003) Exclusion of maltodextrins from phosphatidylcholine multilayers during dehydration: effects on membrane phase behaviour. European Biophysics Journal 32: 96-105.

8. Koster KL, Reisdorph N, Ramsay JL (2003) Changing desiccation tolerance of pea embryo protoplasts during germination. Journal of Experimental Botany 54: 1607-1614.

9. Koster KL, Sommervold CL, Lei YP (1996) The effect of storage temperature on interactions between dehydrated sugars and phosphatidylcholine. Journal of Thermal Analysis 47: 1581-1596

10. Koster KL, Webb MS, Bryant G, Lynch DV (1994) Interactions between soluble sugars and POPC (1-palmitoyl-2-oleoylphosphatidylcholine) during dehydration: vitrification of sugars alters the phase behavior of the phospholipid. Biochimica et Biophysica Acta 1193: 143-150

11. Leopold AC (1986) Membranes, Metabolism and Dry Organisms. Cornell University Press, Ithaca, NY

12. Ramsay JL (2002) Ultrastructure of pea embryonic axes (Pisum sativum L. cv. Alaska) and the associated loss of desiccation tolerance during germination. PhD Dissertation, University of South Dakota.

13. Ramsay JL, Koster KL (2000) Ultrastructure of pea embryonic axes and embryo-derived protoplasts during germination and desiccation. Presented at Plant Biology 2000, the Annual Meeting of the American Society of Plant Physiologists, San Diego, CA

14. Reisdorph NA, Koster KL (1999) The progressive loss of desiccation tolerance in germinating pea (Pisum sativum) seeds. Physiologia Plantarum 105: 266-271

15. Rowen RS (2004) Desiccation tolerance of pea (Pisum sativum L. cv. Alaska) embryo protoplasts: is drying rate dependence due to ROS mediated damage? MS Thesis, University of South Dakota

16. Schipper EL (2000) The effects of the rate of drying on the desiccation tolerance of protoplasts isolated from germinating pea (Pisum sativum L.) seeds. Honors Thesis, University of South Dakota

17. Steponkus PL (1984) Role of the plasma membrane in freezing injury and cold acclimation. Annual Review of Plant Physiology 35: 543-584

18. Steponkus PL, Lynch DV, Uemura M (1990) The influence of cold acclimation on the lipid composition and cryobehaviour of the plasma membrane of isolated rye protoplasts. Philosophical Transactions of the Royal Society of London, B 326: 571-583

19. Steponkus PL, Uemura M, Webb MS (1993) A contrast of the cryostability of the plasma membrane of winter rye and spring oat - two species that widely differ in their freezing tolerance and plasma membrane lipid composition. Advances in Low Temperature Biology 2: 1-67

20. Xiao L, KL Koster (2001) Desiccation tolerance of protoplasts isolated from pea embryos. Journal of Experimental Botany 52: 2105-2114.

21. Walters C, JM Farrant, NW Pammenter, P Berjak (2001a) Desiccation stress and damage. In M Black, HW Pritchard, eds., Desiccation and Plant Survival. CABI Publishing, Oxford, pp 263-291

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