Hald Simon, Nandha Beena, Gallois Patrick, Johnson Giles N
Faculty of Life Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK.
Biochim Biophys Acta. 2008 May;1777(5):433-40. doi: 10.1016/j.bbabio.2008.02.007. Epub 2008 Mar 6.
When plants experience an imbalance between the absorption of light energy and the use of that energy to drive metabolism, they are liable to suffer from oxidative stress. Such imbalances arise due to environmental conditions (e.g. heat, chilling or drought), and can result in the production of reactive oxygen species (ROS). Here, we present evidence for a novel protective process - feedback redox regulation via the redox poise of the NADP(H) pool. Photosynthetic electron transport was studied in two transgenic tobacco (Nicotiana tabacum) lines - one having reduced levels of ferredoxin NADP+-reductase (FNR), the enzyme responsible for reducing NADP+, and the other reduced levels of glyceraldehyde 3-phosphate dehydrogenase (GAPDH), the principal consumer of NADPH. Both had a similar degree of inhibition of carbon fixation and impaired electron transport. However, whilst FNR antisense plants were obviously stressed, with extensive bleaching of leaves, GAPDH antisense plants showed no visible signs of stress, beyond having a slowed growth rate. Examination of electron transport in these plants indicated that this difference is due to feedback regulation occurring in the GAPDH but not the FNR antisense plants. We propose that this reflects the occurrence of a previously undescribed regulatory pathway responding to the redox poise of the NADP(H) pool.
当植物吸收的光能与利用该能量驱动新陈代谢之间出现失衡时,它们容易遭受氧化应激。这种失衡是由环境条件(如高温、低温或干旱)引起的,并会导致活性氧(ROS)的产生。在此,我们提供了一种新型保护过程的证据——通过NADP(H)池的氧化还原平衡进行反馈氧化还原调节。在两个转基因烟草(Nicotiana tabacum)品系中研究了光合电子传递——一个品系中ferredoxin NADP + -还原酶(FNR,负责还原NADP + 的酶)水平降低,另一个品系中甘油醛3 -磷酸脱氢酶(GAPDH,NADPH的主要消耗者)水平降低。两者对碳固定的抑制程度相似,电子传递受损。然而,虽然FNR反义植物明显受到胁迫,叶片出现大面积白化,但GAPDH反义植物除了生长速率减慢外,没有显示出明显的胁迫迹象。对这些植物中电子传递的检测表明,这种差异是由于GAPDH反义植物中发生了反馈调节,而FNR反义植物中没有。我们认为,这反映了一种以前未描述的响应NADP(H)池氧化还原平衡的调节途径的存在。