首页> 外文会议>International Congress of Photosynthesis >LHCII PROTEIN PHOSPHORYLATION IN LEAVES OF ARABIDOPS1S THALIANA MUTANTS DEFICIENT IN NON-PHOTOCHEMICAL QUENCHING
【24h】

LHCII PROTEIN PHOSPHORYLATION IN LEAVES OF ARABIDOPS1S THALIANA MUTANTS DEFICIENT IN NON-PHOTOCHEMICAL QUENCHING

机译:拟南芥叶片中的LHCII蛋白磷酸化缺乏非光化学淬火的突变体

获取原文

摘要

Light reactions generate reactive intermediates and oxygen species that potentially damage photosynthetic machinery, especially in excess light. To prevent the detrimental effects of damaging substances, plants have evolved a number of protection mechanisms -including antioxidant systems and processes for thermal dissipation of light energy. Thermal dissipation in PSII can be measured as quenching of chlorophyll fluorescence in PSII. Characterization of the mutants deficient in non-photochemical quenching (NPQ) has shown that besides the acidification stage of thylakoid lumen, the de-epoxidized xanthophylls and the psbS protein are involved in formation of NPQ (Niyogi et al 1998, Li et al 2000, 2002). npq1 mutants cannot form zeaxanthin in excess light, which results in reduced NPQ and pronounced lipid peroxidation (Havaux & Niyogi 1999), while npq4 mutants typically show strong reduction in NPQ due to deletion or modification of PsbS gene (Li et al 2000, 2002).
机译:光反应产生反应性中间体和氧气物种,可能损坏光合作机,特别是在过量的光线下。为了防止破坏性物质的不利影响,植物已经进化了许多保护机制 - 抗氧化系统和用于光能的热耗散的过程。 PSII中的热耗散可以测量PSII中叶绿素荧光的淬火。缺乏非光化学猝灭(NPQ)的突变体的表征表明,除了甲状腺腔的酸化阶段,除了脱氧曲噻吩和PSBS蛋白涉及NPQ的形成(Niyogi等1998,Li等人2000, 2002)。 NPQ1突变体不能在过量的光线中形成玉米黄蛋白,这导致NPQ和明显的脂质过氧化(Havaux&Niyogi 1999)导致NPQ4突变体由于缺失或修饰PSBS基因而强烈地降低了NPQ(Li等人2000,2002) 。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号