Plants use copper as a cofactor for a wide variety of physiological processes such as photosynthesis, mitochondrial respiration, superoxide scavenging, cell wall metabolism, and ethylene sensing. Low levels of copper in plants can lead to deficiency symptom, which is characterized by slower growth, leaf margins curling and yellowing, damage to apical meristem and reduced fruit production.

In addition to its essentiality, copper is a potentially toxic agent at excess levels. Copper reactivity can lead to the generation of harmful reactive oxygen species that cause severe oxidative damage to cells. Excess copper occurs because of extensive human activities such as mining, industrial particulate emissions, irrigation of untreated or partially untreated industrial and commercial wastewater and the use of Cu-containing pesticide excessive, copper enter the air, soil and water and cause severe environmental pollution. Higher concentrations of Cu can inhibit plant growth, reduce yield, and root activity, thereby changing the absorption of other mineral elements, and reduce photosynthesis by affecting photosystem II. Once the soil becomes Cu contaminated, it can persist for many years because of its low mobility and solubility.

To deal with this dual nature of copper, plants, as well as other organisms, have evolved sophisticated homeostatic networks controlling copper uptake, utilization, and detoxification. The copper regulations systems although less has been studied in plants.

Our group is interesting to better understand the function of COPT1 which is the main copper transporter that is responsible to the uptake of copper ions in the roots and leaves. COPT1 is a homologues protein to the other eukaryotic copper transporters, termed CTR1 family.