Alterations of Gene Expression during the Induction of Freezing Tolerance in a Brassica napus Cell Suspension Culture

Abstract

The ability of crop plants to develop freezing tolerance by cold acclimation is a genetically inherited trait. For example, genes controlling frost tolerance have been identified as being associated with chromosome 5A in winter wheat (Sutka, 1981) and genetic evidence suggest that two dominant epistatic genes may control frost tolerance in Brassica oleracea (Bouwkamp and Honma, 1969). During the attainment of freezing tolerance, plant cells undergo changes resulting in observable altered behavior of their plasmalemma during freezing (Gordon-Kamm and Steponkus, 1984; Singh and Miller, 1985; Pearce and Willison, 1985; Uemura and Yoshida, 1986). It is also known that protein synthesis is required for cold acclimation (Trunova and Zvereva, 1977; Hatano et al., 1976). The manifestation of such synthesis has been observed as increases in protein, membrane lipids, total RNA and soluble sugars (Siminovitch et al., 1968; Gusta and Weiser, 1972). Ultrastructurally, this increased synthetic activity also has been observed as a proliferation of membrane vesicles underlying the plasmalemma (Pomeroy and Siminovitch, 1971; Niki and Sakai, 1981). During acclimation, these vesicles can be seen to be in various states of fusion with the plasmalemma. Cyclohexamide, which inhibits hardening, also prevents the proliferation of such vesicles (Niki and Sakai, 1981).

Contribution No. 1075 of the Plant Research Centre