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苹果花芽遭受冻害时,通过甲基绿—派洛红的染色反应显示细胞核从嗜甲基绿性变为嗜派洛红性,反应DNA从高聚合状态降解到低聚合状态。以核的嗜派洛红性为标志,显示苹果花芽冻害最先发生在花芽基部的维管束,继而是髓细胞,花芽上部的花器官原基分生细胞相对比较抗寒。花芽在寒冬时期(12月中下旬～2月下旬)开始遭到冻害,到早春(3、4月)死亡。抗寒性较弱的‘金冠’花芽在日低温-17℃±开始遭到冻害;抗寒性中等的‘金红’花芽在日低温-20℃±开始受冻;抗寒性强的‘黄太平’在整个越冬过程中绝大部分花芽始终保持正常染色反应,不产生核的嗜派洛红性。
When apple flower buds suffered frost damage, the nuclei changed from methyl green to levaline red through the reaction of methyl green-paliou red, and the DNA was degraded from high polymerization to low polymerization. With the nucleus of Paroxetine marked as red, the apple flower bud frost injury first occurred in the vascular buds at the base of the vascular bundle, followed by the myeloid cells, flower buds above the flower organ primordial mesenchymal cells are relatively cold. Flower buds were frostbite in winter (late-mid-December to late February), and died in early spring (March and April). Cold hardiness’ Golden Delicious’ bud at low temperature -17 ℃ ± began to be frost damage; cold resistance moderate ’golden red’ flower bud at low temperature -20 ℃ ± began to be cold; cold hard ’Huang Taiping During the whole process of winter, most of flower buds always maintain normal dyeing reaction, and do not produce nuclear addictive redness.