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Unravelling the cross-talk between iron starvation and oxidative stress responses highlights the key role of PerR (alr0957) in peroxide signalling in the cyanobacterium Nostoc PCC 7120.
Environmental Microbiology Reports ( IF 3.6 ) Pub Date : 2014-04-09 , DOI: 10.1111/1758-2229.12157
Fan Yingping 1 , Sylvain Lemeille 2 , Emmanuel Talla 1 , Annick Janicki 1 , Yann Denis 3 , Cheng-Cai Zhang 1 , Amel Latifi 1
Affiliation  

The cyanobacterial phylum includes oxygenic photosynthetic prokaryotes of a wide variety of morphologies, metabolisms and ecologies. Their adaptation to their various ecological niches is mainly achieved by sophisticated regulatory mechanisms and depends on a fine cross‐talk between them. We assessed the global transcriptomic response of the filamentous cyanobacterium Nostoc PCC 7120 to iron starvation and oxidative stress. More than 20% of the differentially expressed genes in response to iron stress were also responsive to oxidative stress. These transcripts include antioxidant proteins‐encoding genes that confirms that iron depletion leads to reactive oxygen accumulation. The activity of the Fe‐superoxide dismutase was not significantly decreased under iron starvation, indicating that the oxidative stress generated under iron deficiency is not a consequence of (SOD) deficiency. The transcriptional data indicate that the adaptation of Nostoc to iron‐depleted conditions displays important differences with what has been shown in unicellular cyanobacteria. While the FurA protein that regulates the response to iron deprivation has been well characterized in Nostoc, the regulators in charge of the oxidative stress response are unknown. Our study indicates that the alr0957 (perR) gene encodes the master regulator of the peroxide stress. PerR is a peroxide‐sensor repressor that senses peroxide by metal‐catalysed oxidation.

中文翻译:

弄清铁饥饿和氧化应激反应之间的串扰,凸显了PerR(alr0957)在蓝细菌Nostoc PCC 7120中的过氧化物信号传导中的关键作用。

蓝细菌门包括具有多种形态,新陈代谢和生态的含氧光合原核生物。它们对各种生态位的适应性主要是通过复杂的调节机制来实现的,并且取决于它们之间的良好串扰。我们评估了丝状蓝细菌N ostoc的整体转录反应 PCC 7120可以消除铁的饥饿和氧化应激。响应于铁胁迫的差异表达基因的20%以上也响应氧化应激。这些转录本包括抗氧化剂蛋白编码基因,这些基因证实铁的消耗会导致活性氧的积累。铁饥饿状态下铁超氧化物歧化酶的活性没有显着降低,表明铁缺乏下产生的氧化应激不是(SOD)缺乏的结果。转录数据表明,N ostoc对缺铁条件的适应性与单细胞蓝细菌显示出重要的差异。尽管FurA蛋白可调节铁缺乏的反应,N ostoc是负责氧化应激反应的调节剂,目前尚不清楚。我们的研究表明alr0957(perR)基因编码过氧化物应激的主调节剂。PerR是一种过氧化物传感器阻遏剂,可通过金属催化的氧化来检测过氧化物。
更新日期:2014-04-09
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