DEPOLYMERIZATION OF CORTICAL MICROTUBULES IS NOT A PRIMARY CAUSE OF CHILLING INJURY IN CORN (ZEA-MAYS L CV BLACK MEXICAN SWEET) SUSPENSION-CULTURE CELLS

Cold-induced depolymerization of cortical microtubules were examined in suspension culture cells of corn (Zea mays L. cv Black Mexican Sweet) at various stages of chilling. In an attempt to determine whether microtubule depolymerization contributes to chilling injury, experiments were carried out with and without abscisic acid (ABA) pretreatment, since ABA reduces the severity of chilling injury in these cells. Microtubule depolymerization was detectable after 1 h at 4-degrees-C and became more extensive as the chilling was prolonged. There was little chilling injury after 1 d at 4-degrees-C in either ABA-treated or non-ABA-treated cells. After 3 d at 4-degrees-C, there was about 26% injury for ABA-treated and 40% injury for non-ABA-treated cells, as evaluated by 2,3,5-triphenyl-tetrazolium chloride reduction and by regrowth. After 1 d at 4-degrees-C, less than 10% of cells retained full arrays of microtubules in both ABA-treated and non-ABA-treated cells, the remainder having either partial arrays or no microtubules. After 3 d at 4-degrees-C, about 90% of cells showed complete or almost complete depolymerization of microtubules in both ABA-treated and non-ABA-treated cells. ABA did not stabilize the cortical microtubules against cold-induced depolymerization. In about 66% of ABA-treated cells and 57% of non-ABA-treated cells that had been held at 4-degrees-C for 3 d, repolymerization of cortical microtubules occurred after 3 h at 28-degrees-C. These results argue against the hypothesis that depolymerization of cortical microtubules is a primary cause of chilling injury.