PfsR is a key regulator of iron homeostasis in Synechocystis PCC 6803.
PfsR is a key regulator of iron homeostasis in Synechocystis PCC 6803.
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PfsR 是集胞藻 PCC 6803 中铁稳态的关键调节剂
DOI：
10.1371/journal.pone.0101743
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
He Q
中科院分区：
文献类型：
--
作者：
Cheng D;He Q
铁是许多细胞过程中必不可少的辅因子。海洋中的缺铁影响了包括蓝藻在内的浮游植物的初级生产力。在这项研究中，我们研究了铁稳态的蓝藻集胞藻PCC 6803的PfsR，TetR家族的转录调控因子的功能。与野生型相比，pfsR缺失突变体表现出更强的耐铁限制能力，在铁限制条件下积累了更多的叶绿素a、类胡萝卜素和藻蓝蛋白。突变体还保持更多的光系统I和光系统II复合物比野生型铁剥夺后。此外，在铁限制条件下，pfsR缺失突变体的光系统I和光系统II的活性远高于野生型细胞。铁限制和基因的失活显著影响fut基因（编码三价铁转运蛋白）、feoB（编码亚铁转运蛋白）、bfr基因（编码细菌铁蛋白）、ho基因（编码血红素加氧酶）、isiA（编码叶绿素结合蛋白）和furA（编码三价铁摄取调节剂）的表达，从而增强pfsR的转录。pfsR缺失突变体细胞铁配额在暴露于铁限制之前和之后均高于野生型细胞。电泳迁移率变动分析表明，PfsR绑定到自己的启动子，从而自动调节自己的表达。这些数据表明，PfsR是铁稳态的关键调节剂。
Iron is an essential cofactor in numerous cellular processes. The iron deficiency in the oceans affects the primary productivity of phytoplankton including cyanobacteria. In this study, we examined the function of PfsR, a TetR family transcriptional regulator, in iron homeostasis of the cyanobacterium Synechocystis PCC 6803. Compared with the wild type, the pfsR deletion mutant displayed stronger tolerance to iron limitation and accumulated significantly more chlorophyll a, carotenoid, and phycocyanin under iron-limiting conditions. The mutant also maintained more photosystem I and photosystem II complexes than the wild type after iron deprivation. In addition, the activities of photosystem I and photosystem II were much higher in pfsR deletion mutant than in wild-type cells under iron-limiting conditions. The transcripts of pfsR were enhanced by iron limitation and inactivation of the gene affected pronouncedly expression of fut genes (encoding a ferric iron transporter), feoB (encoding a ferrous iron transporter), bfr genes (encoding bacterioferritins), ho genes (encoding heme oxygenases), isiA (encoding a chlorophyll-binding protein), and furA (encoding a ferric uptake regulator). The iron quota in pfsR deletion mutant cells was higher than in wild-type cells both before and after exposure to iron limitation. Electrophoretic mobility shift assays showed that PfsR bound to its own promoter and thereby auto-regulated its own expression. These data suggest that PfsR is a critical regulator of iron homeostasis.
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影响因子：
2.8
作者：
Ghassemian, M;Straus, NA
通讯作者：
Straus, NA
DOI：
10.1073/pnas.0600927103
发表时间：
2006-05-02
影响因子：
11.1
作者：
Dühring, U;Axmann, IM;Wilde, A
通讯作者：
Wilde, A
影响因子：
64.8
作者：
Becskei, A;Serrano, L
通讯作者：
Serrano, L
影响因子：
2.8
作者：
Chen, CY;Morse, SA
通讯作者：
Morse, SA
影响因子：
3.2
作者：
Fuangthong, M;Herbig, AF;Helmann, JD
通讯作者：
Helmann, JD