Phytochelatin synthases (PCS, EC 2.3.2.15) are cytosolic enzymes, constitutively expressed in the genome of different organisms including Schizosaccharomyces pombe (1), Caenorhabditis elegans (2,3), algae and plants (4). PCS have been explicitly studied with respect to their role and mechanism of action towards heavy metal detoxification (e.g. essential heavy metals such as zinc (Zn) as well as toxic such as cadmium (Cd) (5). Based on studies of Arabidopsis thaliana phytochelatin synthase 1 (AtPCS1), it is recognized that PCS catalyse the formation of thiol rich oligomers, phytochelatins (PCs), from glutathione (GSH) and related thiols in the presence of metal ions (6). Moreover: i) AtPCS1 is involved in the catabolism of GSH-conjugates (7); ii) AtPCS1 is required for pathogen-triggered callose deposition (8); iii) its mRNA is upregulated by a mimic of eubacterial flagellin (8); iv) AtPCS1 expression might be not upregulated by heavy metal toxicity (9), but its transcript abundance in roots increases by deficiency of the micronutrient iron (Fe) (10); v) physiological (homeostatic) Fe concentrations activate the in vitro activity of PCS even in basal land plants (11). The main goal of this study was to determine the AtPCS1-driven response towards Fe deficiency and to establish whether and how AtPCS1 is involved in Fe homeostasis. To do so, we compared the growth, Fe concentration, and the expression of Fe transporter genes in roots and shoots of the A. thaliana cad1-3 mutant lacking functional AtPCS1 and transgenic plants overexpressing AtPCS1 (AtPCS1-OE) vs. wild-type, all grown either under Fe-sufficient or deficient conditions. We found that the cad1-3 mutant accumulated less Fe in roots and was significantly more sensitive to Fe deficiency than wild-type plants. By contrast, AtPCS1-OE lines were more tolerant to Fe deficiency than cad1-3 and wild-type plants. These results were consistent with the expression of Fe transporter genes in different plant lines. A mechanistic model of the role of AtPCS1 in Fe homeostasis will be proposed and discussed.
Phytochelatin synthase 1 regulates iron homeostasis in Arabidopsis thaliana
Luigi Sanità di Toppi
;
2017-01-01
Abstract
Phytochelatin synthases (PCS, EC 2.3.2.15) are cytosolic enzymes, constitutively expressed in the genome of different organisms including Schizosaccharomyces pombe (1), Caenorhabditis elegans (2,3), algae and plants (4). PCS have been explicitly studied with respect to their role and mechanism of action towards heavy metal detoxification (e.g. essential heavy metals such as zinc (Zn) as well as toxic such as cadmium (Cd) (5). Based on studies of Arabidopsis thaliana phytochelatin synthase 1 (AtPCS1), it is recognized that PCS catalyse the formation of thiol rich oligomers, phytochelatins (PCs), from glutathione (GSH) and related thiols in the presence of metal ions (6). Moreover: i) AtPCS1 is involved in the catabolism of GSH-conjugates (7); ii) AtPCS1 is required for pathogen-triggered callose deposition (8); iii) its mRNA is upregulated by a mimic of eubacterial flagellin (8); iv) AtPCS1 expression might be not upregulated by heavy metal toxicity (9), but its transcript abundance in roots increases by deficiency of the micronutrient iron (Fe) (10); v) physiological (homeostatic) Fe concentrations activate the in vitro activity of PCS even in basal land plants (11). The main goal of this study was to determine the AtPCS1-driven response towards Fe deficiency and to establish whether and how AtPCS1 is involved in Fe homeostasis. To do so, we compared the growth, Fe concentration, and the expression of Fe transporter genes in roots and shoots of the A. thaliana cad1-3 mutant lacking functional AtPCS1 and transgenic plants overexpressing AtPCS1 (AtPCS1-OE) vs. wild-type, all grown either under Fe-sufficient or deficient conditions. We found that the cad1-3 mutant accumulated less Fe in roots and was significantly more sensitive to Fe deficiency than wild-type plants. By contrast, AtPCS1-OE lines were more tolerant to Fe deficiency than cad1-3 and wild-type plants. These results were consistent with the expression of Fe transporter genes in different plant lines. A mechanistic model of the role of AtPCS1 in Fe homeostasis will be proposed and discussed.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
