Deficiency and toxicity of nanomolar copper in low irradiance-A physiological and metalloproteomic study in the aquatic plant Ceratophyllum demersum

- Environmentally relevant toxicity and limitation of Cu were investigated.
- Copper > 50nM replaces Mg in the LHCII‐trimers.
- Deficiency causes decreased electron flow through PSII via lack of plastocyanin.
- Of all metabolic pathways, photosynthesis was most affected by Cu toxicity.
- Detection of Cu in the Chl peaks of LHCII suggests the generation of [Cu]‐Chl.

Essential trace elements (Cu2+, Zn2+, etc) lead to toxic effects above a certain threshold, which is a major environmental problem in many areas of the world. Here, environmentally relevant sub-micromolar concentrations of Cu2+ and simulations of natural light and temperature cycles were applied to the aquatic macrophyte Ceratophyllum demersum a s a model for plant shoots. In this low irradiance study resembling non‐summer conditions, growth was optimal in the range 7.5-35 nM Cu, while PSII activity (Fv/Fm) was maximal around 7.5 nM Cu. Damage to the light harvesting complex of photosystem II (LHCII) was the first target of Cu toxicity (>50 nM Cu) where Cu replaced Mg in the LHCII-trimers. This was associated with a subsequent decrease of Chl a as well as heat dissipation (NPQ). The growth rate was decreased from the first week of Cu deficiency. Plastocyanin malfunction due to the lack of Cu that is needed for its active centre was the likely cause of diminished electron flow through PSII (ΦPSII). The pigment decrease added to the damage in the photosynthetic light reactions. These mechanisms ultimately resulted in decrease of starch and oxygen production.