Abstract

Summary The molecular basis of chilling injury (CI) was investigated in mature-green tomato ( Lycopersicon esculentum Mill. cv. Caruso) fruit. Present evidence identifies the cellular membranes, particularly those of the chloroplast, as likely targets of the injury. Recent literature indicates reduced galactolipid (GL) content in tomato pericarp, with little change in phospholipid (PL) content and fatty acid composition during exposure to low temperature. Wanner et al. (1991) report simultaneous loss of GLand accumulation of polyunsaturated phosphatidylcholine (PC) in senescent barley leaves. The present paper shows a similar shift of PC toward less saturated molecular species during 18 d of chilling at 1 °C and to a lesser extent during ripening at 20 °C. In contrast the molecular species of phosphatidylethanolamine (PE) showed the opposite trend during ripening and were little affected by low temperature. Diglyceride (DG) composition remained essentially unchanged under these conditions. Four days after the fruits were transferred to 20 °C, the trend toward polyunsaturation of PC had been partly reversed, while the molecular species of PE and DGs were not modified during the postchilling period. The molecular species profile of DGs was more similar to that of PLs than to that of GLs. The accumulation of polyunsaturated PCs during chilling and their postchilling degradation may explain why CI symptoms appear mainly after transfer of the fruits to a higher temperature.

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