In vivo modulation of nonphotochemical exciton quenching (NPQ) by regulation of the chloroplast ATP synthase
In vivo modulation of nonphotochemical exciton quenching (NPQ) by regulation of the chloroplast ATP synthase
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DOI：
10.1073/pnas.182427499
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发表时间：
2002-10-01
影响因子：
11.1
通讯作者：
Kramer, DM
中科院分区：
文献类型：
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作者：
Kanazawa, A;Kramer, DM
激发能的非光化学猝灭（NPQ）可以保护高等植物的光合机制免受光损伤，它是由光诱导质子泵送导致的类囊体腔酸化引发的，这也驱动了ATP的合成。很明显，NPQ的敏感性响应于生理条件的变化而被调节，但是这种调节的机制仍然不清楚。有证据表明，在完整的烟草或拟南芥叶片，NPQ调制响应CO2水平的变化主要发生在CF 0-CF 1 ATP合酶的质子（g（H）（+））的电导率的改变。在给定的质子通量下，降低gH+将增加类囊体质子动力（pmf），从而降低管腔pH值并有助于NPQ的活化。结果发现，当大气CO2从2，000 ppm降低到0 ppm时，g（H）（+）降低约5倍可以解释NPQ调节的主要原因。数据显示，g（H）（+）是动力学控制的，而不是由DeltaG（ATP）的积累所强加的。进一步的结果表明，ATP合酶γ亚基硫醇的氧化还原状态不是改变g（H）（+）的原因。提出了一个工作模型，其中g（H）（+）由基质代谢物水平调节，可能是由无机磷酸盐。
Nonphotochemical quenching (NPQ) of excitation energy, which protects higher plant photosynthetic machinery from photodamage, is triggered by acidification of the thylakoid lumen as a result of light-induced proton pumping, which also drives the synthesis of ATP. It is clear that the sensitivity of NPQ is modulated in response to changing physiological conditions, but the mechanism for this modulation has remained unclear. Evidence is presented that, in intact tobacco or Arabidopsis leaves, NPQ modulation in response to changing CO2 levels occurs predominantly by alterations in the conductivity of the CF0-CF1 ATP synthase to protons (g(H)(+)). At a given proton flux, decreasing gH+ will increase transthylakoid proton motive force (pmf), thus lowering lumen pH and contributing to the activation of NPQ. It was found that an approximate to5-fold decrease in g(H)(+) could account for the majority of NPQ modulation as atmospheric CO2 was decreased from 2,000 ppm to 0 ppm. Data are presented that g(H)(+) is kinetically controlled, rather than imposed thermodynamically by buildup of DeltaG(ATP). Further results suggest that the redox state of the ATP synthase gamma-subunit thiols is not responsible for altering g(H)(+). A working model is proposed wherein g(H)(+) is modulated by stromal metabolite levels, possibly by inorganic phosphate.