Abstract
Copper is an essential element involved in fundamental processes like respiration and photosynthesis. However, it becomes toxic at high concentration, which has forced organisms to control its cellular concentration. We have recently described a copper resistance system in the cyanobacterium Synechocystis sp. PCC 6803, which is mediated by the two-component system, CopRS, a RND metal transport system, CopBAC and a protein of unknown function, CopM. Here, we report the transcriptional responses to copper additions at non-toxic (0.3 µM) and toxic concentrations (3 µM) in the wild type and in the copper sensitive copR mutant strain. While 0.3 µM copper slightly stimulated metabolism and promoted the exchange between cytochrome c6 and plastocyanin as soluble electron carriers, the addition of 3 µM copper catalyzed the formation of ROS, led to a general stress response and induced expression of Fe-S cluster biogenesis genes. According to this, a double mutant strain copRsufR, which expresses constitutively the sufBCDS operon, tolerated higher copper concentration than the copR mutant strain, suggesting that Fe-S clusters are direct targets of copper toxicity in Synechocystis. In addition we have also demonstrated that InrS, a nickel binding transcriptional repressor that belong to the CsoR family of transcriptional factor, was involved in heavy metal homeostasis, including copper, in Synechocystis. Finally, global gene expression analysis of the copR mutant strain suggested that CopRS only controls the expression of copMRS and copBAC operons in response to copper.
Highlights
Copper is an essential oligoelement that is required as a cofactor for a number of cuproenzymes including amine oxidases, cytochrome c oxidases, laccases, methane monooxygenases, multicopper oxidases, nitrite oxidases, plastocyanin, superoxide dismutases and tyrosinases
In this work we have reported the transcriptional profiles of the WT and a copR mutant (COP4) Synechocystis strains in response to low and high copper concentration treatments
The low copper treatment (0.3 mM) revealed a slight induction of cell anabolism, mainly cyclic photosynthesis, through up-regulation of genes related to energy metabolism and translation and repression of Photosystem II (PSII) genes (Fig. 7)
Summary
Copper is an essential oligoelement that is required as a cofactor for a number of cuproenzymes including amine oxidases, cytochrome c oxidases, laccases, methane monooxygenases, multicopper oxidases, nitrite oxidases, plastocyanin, superoxide dismutases and tyrosinases. These proteins are involved in diverse cellular processes such as energy transduction, iron mobilization and oxidative stress response [1,2]. PCC 6803 (hereafter Synechocystis), in which Cu(I), the predominant intracellular species [5], interferes with the function and/or stability of catalytic Fe-S clusters, damaging essential enzymes [6,7,8] All these have forced all living organisms to develop homeostatic mechanisms to tightly control cellular copper pools
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