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

A unique ferredoxin acts as a player in the low-iron response of photosynthetic organisms.
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DOI:
10.1073/pnas.1810379115
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发表时间:
2018-12-18
影响因子:
11.1
通讯作者:
Hanke GT
Hanke GT
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Schorsch M;Kramer M;Goss T;Eisenhut M;Robinson N;Osman D;Wilde A;Sadaf S;Brückler H;Walder L;Scheibe R;Hase T;Hanke GT

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铁限制了光合作用生物的生长,特别是在海洋环境中。因此,了解光合作用生物对铁浓度变化的反应对农业和生物技术很重要。我们已经确定了一种对光合作用细菌(蓝藻)中铁浓度变化做出正确反应所必需的蛋白质。这种蛋白质以前被注释为光合作用的电子转移成分,称为FED2,包含一个铁−硫簇。我们测试了Fed2,发现它不能进行光合作用的电子传递。相应的基因是必不可少的,并且在蓝藻、藻类和高等植物中高度保守。通过具体干扰它的功能,我们可以证明它在转录后水平上对低铁反应是必不可少的。铁长期限制水生光合作用,特别是在海洋环境中,因此,正确认识和维持包括蓝藻在内的光合作用细菌中的铁稳态具有全球意义。已经确定了多种适应机制、响应启动子和转录后调节因子,使蓝藻能够对不断变化的铁浓度做出反应。然而,许多因素仍然不清楚,特别是细胞内铁状态是如何被感知的。在这里,我们描述了一种蓝藻铁还蛋白(Fed2),具有独特的C-端延伸,在铁感知中发挥作用。FED2同系物在从蓝藻到高等植物的光合作用生物中高度保守,虽然它们属于植物型铁氧还蛋白家族的[2Fe-2S]光合作用电子载体,但它们不参与光合作用的电子传递。由于Fed2的缺失似乎是致命的,我们开发了一个C末端截断系统来减弱蛋白质的功能。受干扰的Fed2功能导致叶绿素积累减少,这在缺铁的介质中被夸大,不同的截断导致对低铁的反应被夸大或减弱。尽管如此,铁的浓度在所有截断突变体中保持不变,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无法在转录和蛋白水平上积累。相比之下,与ISIA共享操纵子的ISIB的丰度不受Fed2功能丧失的影响,将Fed2在铁感知中的作用位置定位于转录后调控水平。
Iron limits the growth of photosynthetic organisms, especially in marine environments. Understanding the response of photosynthetic organisms to changing iron concentrations is therefore important for agriculture and biotechnology. We have identified a protein that is essential for the correct response to changing iron concentrations in photosynthetic bacteria (cyanobacteria). This protein was previously annotated as an electron transfer component of photosynthesis, called Fed2, and contains an iron−sulfur cluster. We tested Fed2, and found that it cannot act in photosynthetic electron transport. The corresponding gene is essential, and is highly conserved between cyanobacteria, algae, and higher plants. By specifically perturbing its function, we could show that it is essential for the low-iron response at the posttranscriptional level. 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.
DOI: 10.1073/pnas.0600927103
发表时间: 2006-05-02
影响因子: 11.1
作者:
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期刊: NATURE
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影响因子: 7.4
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发表时间: 2003-10-24
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发表时间: 2013-01-01
影响因子: 3.3
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