Desiccation tolerance is one of the most fundamental properties of seeds. It is acquired late in seed development and is considered necessary for the completion of the plant's life cycle, as an adaptive strategy to enable seed survival during storage or environmental stress, and to ensure better dissemination of the species. The role of water status in desiccated tissues and problems related to testing tolerance in seeds are reviewed. The molecular mechanisms of desiccation tolerance has received extensive consideration only during this past decade. There is a general consensus that desiccation tolerance involves the protection of cellular membranes from the deleterious effect of water removal and the resultant necessity to maintain the bilayer structure in the absence of an aqueous environment. Therefore, some aspects of desiccation-induced membrane injury are described. Several strategies for coping with cellular desiccation have been identified the presence of high amounts of non-reducing sugars, the efficiency of free radical-scavenging systems and the expression of desiccation- and/or ABA-regulated genes. These molecular mechanisms allowing cellular protection are reviewed together with their respective role in dessication tolerance. It is concluded that desiccation tolerance is not likely to be ascribed to a single mechanism but rather to a multifactorial property in which each component is equally critical.

Activated oxygen or oxygen free radicals have been implicated in a number of physiological disorders in plants including freezing injury. Superoxide dismutase (SOD) catalyzes the dismutation of superoxide into O2 and H202 and thereby reduces the titer of activated oxygen molecules in the cell. To further examine the relationship between oxidative and freezing stresses, the expression of SOD was modified in transgenic alfalfa (Medicago safiva 1.). The Mn-SOD cDNA from Nicotiana plumbaginifolia under the control of the cauliflower mosaic virus 35s promoter was introduced into alfalfa using Agrobacferium tumefaciens-mediated transformation. Two plasmid vectors, pMitSOD and pChlSOD, contained a chimeric Mn-SOD construct with a transit peptide for targeting to the mitochondria or one for targeting to the chloroplast, respectively. The putatively transgenic plants were selected for resistance to kanamycin and screened for neomycin phosphotransferase activity and the presence of an additional Mn-SOD isozyme. Detailed analysis of a set of four selected transformants indicated that some had enhanced SOD activity, increased tolerante to the diphenyl ether herbicide, acifluorfen, and increased regrowth after freezing stress. l h e F1 progeny of one line, RA3-ChlSOD-30, were analyzed by SOD isozyme activity, by polymerase chain reaction for the Mn-SOD gene, and by polymerase chain reaction for the neo gene. RA3-ChlSOD-30 had three sites of insertion of pChlSOD, but only one gave a functional Mn-SOD isozyme; the other two were apparently partia1 insertions. The progeny with a functional Mn-SOD transgene had more rapid regrowth following freezing stress than those progeny lacking the functional Mn-SOD transgene, suggesting that Mn-SOD serves a protective role by minimizing oxygen free radical production after freezing stress.Activated oxygen species such as superoxide, hydrogen peroxide, and hydroxyl radical are associated with a number of physiological disorders in plants. Although activated oxygen is produced as a by-product of normal cell metabolism, its levels are enhanced by exposure to chemical and environ-'

Transgenic alfalfa (Medicago safiva) expressing Mn-superoxide dismutase cDNA tended to have reduced injury from water-deficit stress as determined by chlorophyll fluorescence, electrolyte leakage, and regrowth from crowns. A 3-year field trial indicated that yield and survival of transgenic plants were significantly improved, supporting the hypothesis that tolerance of oxidative stress is important in adaptation to field environments.Many of the degenerative reactions associated with severa1 biotic, abiotic, and xenobiotic stresses are mediated by toxic, reactive oxygen intermediates formed from superoxide, such as the hydroxyl radical (Scandalios, 1993; Allen, 1995). These stresses include the herbicide paraquat (Bowler et al., 1991;Herouart et al., 1993), ozone (Van Camp et al., 1994), anoxia (Monk et al., 1989), pathogens (Mehdy, 1994), desiccation (Senaratna et al., 1985a(Senaratna et al., , 1985b, and freezing (Kendall and McKersie, 1989;McKersie et al., 1993). The mechanisms to detoxify oxygen radicals are varied, and the complex interactions among the antioxidants in different subcellular compartments, cells, and tissues are only now being elucidated. SOD is an essential component of these defense mechanisms because it dismutates two superoxide radicals to produce hydrogen peroxide and oxygen (Scandalios, 1993; Allen, 1995). The observation that water deficiency caused the chloroplasts of wheat (Trificum aestivum L.) to reduce oxygen to superoxide because of a drought-impaired electron transport system (Price et al., 1989) prompted us to hypothesize that plants overexpressing SOD might have improved tolerance of water deficit. Previously, an Mn-SOD cDNA from Nicotiana plumbaginifolia was introduced into alfalfa; the primary transformants and their F, transgenic progeny showed increased survival and vigor after exposure to sublethal freezing stress . We now report the results of two further experiments with these transgenic plants, indicating that manipulation of genes associated with oxidative stress tolerance can also improve survival and vigor after exposure to water deficit in controlled environments and over three winters in natural field environments. These preliminary studies indicate that a rigorous analysis of the oxidative stress response will aid in the genetic improvement of environmental stress tolerante in crop plants.

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