In land plants plastocyanin is indispensable and therefore copper (Cu) availability is a prerequisite for growth. When Cu supply is limited, higher plants prioritize the Cu delivery to plastocyanin by down-regulation of other Cu proteins. Arabidopsis has two plastocyanin genes (PETE1 and PETE2). PETE2 is the predominant isoform in soil-grown plants and in hydroponic cultures it is accumulated in response to Cu addition. It functions as a Cu sink when more Cu is available, in addition to its role as an electron carrier. PETE1 is not affected by Cu feeding and it is the isoform that drives electron transport under Cu-deficiency. Cu feeding rescued the defect in photosystem II electron flux (Phi(PSII)) in the pete1 mutant whereas Phi(PSII) was not changed in the pete2 mutant as Cu was added. Plants with mutations in the plastocyanin genes had altered Cu homeostasis. The pete2 mutant accumulated more Cu/Zn superoxide dismutase (CSD2 and CSD1) and Cu chaperone (CCS) whereas the pete1 mutant accumulated less. On the other hand, less iron superoxide dismutase (FeSOD) and microRNA398b were observed in the pete2 mutant, whereas more were accumulated in the pete1 mutant. Our data suggest that plastocyanin isoforms are different in their response to Cu and the absence of either one changes the Cu homeostasis. Also a small amount of plastocyanin is enough to support efficient electron transport and more PETE2 is accumulated as more Cu is added, presumably, to buffer the excess Cu.