Figure 10.

A working model for the KIN17-SPL7 node function under Cu deficiency. ROS are constantly generated in plant cells, especially due to PETC activity. Increased levels of ROS cause DNA damage and eventually result in abrogation of cell proliferation. The availability of Cu determines which enzymatic antioxidant response plants activate to counteract the deleterious effect of ROS. Whereas Cu is used to fulfill Cu-dependent antioxidant responses led by the Cu/Zn SOD during Cu sufficiency, it must be economized for fundamentally important Cu proteins during Cu-deficient periods. Consequently, the SPL7 transcription factor promotes a Cu-uptake and -redistribution strategy to preferentially allocate Cu toward PC and thus maintain the PETC as functional. Additionally, SPL7 also coordinates the Cu/Zn SOD substitution by the Fe SOD isoform to ensure a Cu-independent antioxidant response. In the case of high ROS levels, we propose that Arabidopsis KIN17 acts at three levels to counteract this scenario: (1) KIN17 would associate with SPL7 either to enhance the Cu-starvation response and reinforce the cellular antioxidant system or to protect additional yet-unknown Cu-dependent processes related to plant growth and development; (2) KIN17 would converge, directly or indirectly, with SPL7 to maintain some Cu-independent antioxidant system; and (3) KIN17 would also be directly involved in repairing DNA lesions, as reported in mammals.