膜脂不饱和化加速光合作用从低温光抑制中的恢复：一种耐寒机制。
The recovery of photosynthesis from low-temperature photoinhibition is accelerated by the unsaturation of membrane lipids: a mechanism of chilling tolerance.
作者信息
Gombos Z, Wada H, Murata N
机构信息
Department of Regulation Biology, National Institute for Basic Biology, Okazaki, Japan.
出版信息
Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8787-91. doi: 10.1073/pnas.91.19.8787.
Abstract
In a previous study of mutants in fatty-acid desaturation of Synechocystis PCC6803, it was demonstrated that the photoinhibition of photosynthesis at low temperature in vivo is tolerated by cells as a result of the unsaturation of glycerolipids of thylakoid membranes. Since the extent of photoinhibition of photosynthesis in vivo depends on a balance between the photoinduced inactivation and the recovery from the photoinhibited state, an examination was made of the effects of the unsaturation of membrane lipids on these processes. It appears that the unsaturation of the membrane lipids does not affect the inactivation process but accelerates the recovery process and, moreover, that the apparent increase in the photoinhibition in vivo of photosynthesis at low temperature is caused by a depressed rate of recovery at low temperature.
摘要
在先前对集胞藻PCC6803脂肪酸去饱和突变体的研究中，已证明体内低温下光合作用的光抑制可被细胞耐受，这是类囊体膜甘油脂不饱和化的结果。由于体内光合作用光抑制的程度取决于光诱导失活与从光抑制状态恢复之间的平衡，因此研究了膜脂不饱和化对这些过程的影响。似乎膜脂的不饱和化并不影响失活过程，而是加速了恢复过程，此外，低温下体内光合作用光抑制的明显增加是由低温下恢复速率降低所致。
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