PfsR Is a Key Regulator of Iron Homeostasis in <i>Synechocystis</i> PCC 6803

<div><p>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 <i>Synechocystis</i> PCC 6803. Compared with the wild type, the <i>pfsR</i> 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 <i>pfsR</i> deletion mutant than in wild-type cells under iron-limiting conditions. The transcripts of <i>pfsR</i> were enhanced by iron limitation and inactivation of the gene affected pronouncedly expression of <i>fut</i> genes (encoding a ferric iron transporter), <i>feoB</i> (encoding a ferrous iron transporter), <i>bfr</i> genes (encoding bacterioferritins), <i>ho</i> genes (encoding heme oxygenases), <i>isiA</i> (encoding a chlorophyll-binding protein), and <i>furA</i> (encoding a ferric uptake regulator). The iron quota in <i>pfsR</i> 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.</p>