Tiku P E, Gracey A Y, Macartney A I, Beynon R J, Cossins A R
Department of Environmental and Evolutionary Biology, University of Liverpool, UK.
Science. 1996 Feb 9;271(5250):815-8. doi: 10.1126/science.271.5250.815.
Poikilothermic animals respond to chronic cold by increasing phosphoglyceride unsaturation to restore the fluidity of cold-rigidified membranes. Despite the importance of this compensatory response, the enzymes involved have not been clearly identified, and the mechanisms that control their activity are unknown. In carp liver, cold induces an 8- to 10-fold increase in specific activity of the microsomal stearoyl coenzyme A desaturase. Cold-induced up-regulation of gene transcription resulted in a 10-fold increase in desaturase transcript amounts after 48 to 60 hours. However, this increase was preceded by the activation of latent desaturase, probably by a posttranslational mechanism. These two mechanisms may act sequentially to match desaturase expression to the demands imposed by a progressive decrease in temperature.
变温动物通过增加磷酸甘油酯不饱和度来应对长期寒冷,以恢复冷硬化膜的流动性。尽管这种补偿反应很重要,但其中涉及的酶尚未明确鉴定,控制其活性的机制也不清楚。在鲤鱼肝脏中,寒冷会使微粒体硬脂酰辅酶A去饱和酶的比活性增加8到10倍。寒冷诱导的基因转录上调导致48至60小时后去饱和酶转录本数量增加10倍。然而,这种增加之前是潜伏去饱和酶的激活,可能是通过翻译后机制。这两种机制可能依次起作用,以使去饱和酶表达与温度逐渐降低所带来的需求相匹配。