Wada H, Gombos Z, Murata N
National Institute for Basic Biology, Okazaki, Japan.
Nature. 1990 Sep 13;347(6289):200-3. doi: 10.1038/347200a0.
The sensitivity (or tolerance) of plants to chilling determines their choice of natural habitat and also limits the worldwide production of crops. Although the molecular mechanism for chilling sensitivity has long been debated, no definitive conclusion has so far been reached about its nature. A probable hypothesis, however, is that chilling injury is initiated by phase transition of lipids of cellular membranes, as demonstrated for cyanobacteria, which serve as a model system for the plant cells. Because the phase transition temperature depends on the degree of unsaturation of fatty acids of the membrane lipids, it is predicted that the chilling tolerance of plants can be altered by genetically manipulating fatty-acid desaturation by introducing double bonds into fatty acids of membrane lipids. Here we report the cloning of a gene for the plant-type desaturation (termed desA). The introduction of this gene from a chilling-resistant cyanobacterium, Synechocystis PCC6803, into a chilling-sensitive cyanobacterium, Anacystis nidulans, increases the tolerance of the recipient to low temperature.
植物对低温的敏感性（或耐受性）决定了它们对自然栖息地的选择，也限制了全球农作物的产量。尽管长期以来人们一直在争论低温敏感性的分子机制，但迄今为止尚未就其本质得出明确结论。然而，一个可能的假说是，低温伤害是由细胞膜脂质的相变引发的，这在作为植物细胞模型系统的蓝细菌中得到了证明。由于相变温度取决于膜脂脂肪酸的不饱和度，因此预计可以通过将双键引入膜脂脂肪酸中来对脂肪酸去饱和进行基因操作，从而改变植物的耐冷性。在此，我们报告了一个植物型去饱和基因（称为desA）的克隆。将这个来自抗寒蓝细菌集胞藻PCC6803的基因导入对低温敏感的蓝细菌盘状裂须藻中，可提高受体对低温的耐受性。
