Naranjo Belén, Diaz-Espejo Antonio, Lindahl Marika, Cejudo Francisco Javier
Instituto de Bioquímica Vegetal y Fotosíntesis, Universidad de Sevilla and CSIC, Avda Américo Vespucio, 49, 41092-Sevilla, Spain.
Instituto de Recursos Naturales y Agrobiología de Sevilla, CSIC, Avda Reina Mercedes, 10, 41012-Sevilla, Spain.
J Exp Bot. 2016 Mar;67(6):1951-64. doi: 10.1093/jxb/erw017. Epub 2016 Feb 2.
Redox regulation plays a central role in the adaptation of chloroplast metabolism to light. Extensive biochemical analyses in vitro have identified f-type thioredoxins (Trxs) as the most important catalysts for light-dependent reduction and activation of the enzymes of the Calvin-Benson cycle. However, the precise function of type f Trxs in vivo and their impact on plant growth are still poorly known. To address this issue we have generated an Arabidopsis thaliana double knock-out mutant, termed trxf1f2, devoid of both f1 and f2 Trxs. Despite the essential function previously proposed for f-type Trxs, the visible phenotype of the trxf1f2 double mutant was virtually indistinguishable from the wild type when grown under a long-day photoperiod. However, the Trx f-deficient plants showed growth inhibition under a short-day photoperiod which was not rescued at high light intensity. The absence of f-type Trxs led to significantly lower photosynthetic electron transport rates and higher levels of non-photochemical energy quenching. Notably, the Trx f null mutant suffered from a shortage of photosystem I electron acceptors and delayed activation of carbon dioxide fixation following a dark-light transition. Two redox-regulated Calvin-Benson cycle enzymes, fructose 1,6-bisphosphatase (FBPase) and Rubisco activase, showed retarded and incomplete reduction in the double mutant upon illumination, compared with wild-type plants. These results show that the function of f-type Trxs in the rapid activation of carbon metabolism in response to light is not entirely compensated for by additional plastid redox systems, and suggest that these Trxs have an important role in the light adjustment of photosynthetic metabolism.
氧化还原调节在叶绿体代谢对光的适应过程中起着核心作用。体外广泛的生化分析已确定f型硫氧还蛋白(Trxs)是卡尔文-本森循环中酶的光依赖性还原和激活的最重要催化剂。然而,f型Trxs在体内的确切功能及其对植物生长的影响仍知之甚少。为了解决这个问题,我们构建了一个拟南芥双敲除突变体,称为trxf1f2,它缺失f1和f2 Trxs。尽管之前提出f型Trxs具有重要功能,但在长日照光周期下生长时,trxf1f2双突变体的可见表型与野生型几乎没有区别。然而,Trx f缺陷型植株在短日照光周期下表现出生长抑制,且在高光强下无法恢复。f型Trxs的缺失导致光合电子传递速率显著降低,非光化学能量猝灭水平升高。值得注意的是,Trx f缺失突变体在暗-光转换后存在光系统I电子受体短缺和二氧化碳固定激活延迟的问题。与野生型植株相比,两种氧化还原调节的卡尔文-本森循环酶,果糖1,6-二磷酸酶(FBPase)和Rubisco活化酶,在双突变体光照后显示出还原延迟和不完全。这些结果表明,f型Trxs在响应光时快速激活碳代谢的功能不能完全被其他质体氧化还原系统所补偿,并表明这些Trxs在光合代谢的光调节中具有重要作用。