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PNAS Plus: A unique ferredoxin acts as a player in the low-iron response of photosynthetic organisms

机译:PNAS Plus:独特的铁氧还蛋白在光合生物的低铁反应中发挥作用

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摘要

Iron chronically limits aquatic photosynthesis, especially in marine environments, and the correct perception and maintenance of iron homeostasis in photosynthetic bacteria, including cyanobacteria, is therefore of global significance. Multiple adaptive mechanisms, responsive promoters, and posttranscriptional regulators have been identified, which allow cyanobacteria to respond to changing iron concentrations. However, many factors remain unclear, in particular, how iron status is perceived within the cell. Here we describe a cyanobacterial ferredoxin (Fed2), with a unique C-terminal extension, that acts as a player in iron perception. Fed2 homologs are highly conserved in photosynthetic organisms from cyanobacteria to higher plants, and, although they belong to the plant type ferredoxin family of [2Fe-2S] photosynthetic electron carriers, they are not involved in photosynthetic electron transport. As deletion of fed2 appears lethal, we developed a C-terminal truncation system to attenuate protein function. Disturbed Fed2 function resulted in decreased chlorophyll accumulation, and this was exaggerated in iron-depleted medium, where different truncations led to either exaggerated or weaker responses to low iron. Despite this, iron concentrations remained the same, or were elevated in all truncation mutants. Further analysis established that, when Fed2 function was perturbed, the classical iron limitation marker IsiA failed to accumulate at transcript and protein levels. By contrast, abundance of IsiB, which shares an operon with isiA, was unaffected by loss of Fed2 function, pinpointing the site of Fed2 action in iron perception to the level of posttranscriptional regulation.
机译:铁长期限制了水生物的光合作用,特别是在海洋环境中,因此,对包括蓝细菌在内的光合细菌中铁稳态的正确认识和维持具有全球意义。已经确定了多种适应性机制,响应性启动子和转录后调节剂,它们使蓝细菌能够响应不断变化的铁浓度。然而,许多因素仍然不清楚,特别是如何在细胞内感知铁的状态。在这里,我们描述了具有独特的C末端延伸的蓝细菌铁氧还蛋白(Fed2),它在铁感知中起着重要作用。 Fed2同源物在从蓝细菌到高等植物的光合生物中高度保守,尽管它们属于[2Fe-2S]光合电子载体的植物型铁氧还蛋白家族,但它们不参与光合电子的运输。由于fed2的删除似乎具有致命性,因此我们开发了C端截短系统来减弱蛋白质功能。 Fed2功能紊乱导致叶绿素积累减少,这在缺铁的培养基中被夸大,不同的截短导致对低铁的反应过大或减弱。尽管如此,所有截短突变体中的铁浓度仍保持不变或升高。进一步的分析表明,当Fed2功能受到干扰时,经典的铁限制标记IsiA无法在转录本和蛋白质水平上积累。相比之下,与isaA共享一个操纵子的大量IsiB不受Fed2功能丧失的影响,从而将Fed2在铁质感知中的作用位点精确定位到转录后调控水平。

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