Seedlings of winter wheat ( Tnticum aestivum L. cv. Kharkov) were acclimated at 2 C in the dark in the presence of two inhibitors of linolenic acid synthesis, 4-chloro-5(dimethylamino)2-phenyl-3(2H)pyridazinone-(BASF 13-338) and 4-chloro-5(dimethylamino)-2(a,a,a-trifluoro-m-tolyl)-3(2H)pyridazinone (Sandoz 6706). Although the increase in the proportion of linolenic acid generally observed at low temperature was completely inhibited, the development of freezing tolerance was unaffected. These results demonstrated that an enrichment in linolenic acid is not a prerequisite for low temperature acclimation. Willemot (16) observed that when wheat plants were pretreated with an inhibitor of linolenic acid synthesis (BASF 13-338)2 prior to cold acclimation, both the accumulation of linolenic acid and the development of freezing tolerance were completely inhibited. He concluded that low temperature stimulation of linolenic acid synthesis was a necessary prerequisite to the development of freezing resistance even though it was not the factor responsible for the difference in tolerance observed among the various strains of wheat studied previously (3, 17). Willemot (16) also found that BASF 13-338 inhibited the increases in both dry weight and phospholipid content generally associated with low temperature hardening (13). This observation, coupled with the considerable evidence (6, 11) demonstrating that pyridazinone herbicides inhibit chloroplast function, may be an indication that a reduced level of photosynthetic carbon, and not the inhibition of linolenic acid synthesis, is the causal factor inhibiting cold hardening. The
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