Fig. 8

Schematic model for the (in)activation of SPL7 and the subsequent regulations under Cd and Cu exposure. Cd exposure (orange colored) elicits a Cu deficiency response through the activation of SPL7. Active SPL7 binds to GTAC motifs in the promoters of several Cu transporters, cupro-miRNAs and other genes like FSD1 thereby inducing their expression and decreasing miRNA target transcription. This Cu deficiency response, resulting in an increased Cu uptake and reallocation of Cu to plastocyanin, is required for basal Cd tolerance. The Cd-induced FSD1 expression counterbalances the decrease in CSD1/2 transcript levels to maintain the antioxidative defence against superoxide radicals. Conversely, Cu toxicity (purple colored) inactivates SPL7 resulting in decreased transcription levels of all these SPL7-regulated genes. The regulations of all cupro-miRNA targets are not always clear (indicated by the dotted arrows) since they are also subjected to other SPL7-independent regulation mechanisms. Interestingly, when Cd exposure is combined with extra Cu (green colored), Cu homeostasis remains unaltered in the leaves, resulting in neither Cd-induced Cu deficiency responses nor Cu toxicity responses in the leaves