C/N-interactions: Regulation of nitrate reduction by photosynthesis

Abstract

Primary products of nitrate reduction are nitrite, N-oxides and ammonium, which may become toxic when accumulated. Therfore, reduction of nitrate in the cytosol and consumption of nitrite and ammonium in the plastids have to be synchronized. Cells have developped several regulatory mechanisms to achieve this goal. Reduction of nitrate in the cytosol is controlled by a) regulation of nitrate reductase (NR) mRNA and protein synthesis b) modulation of the activity of NR by protein phosphorylation and 14-3-3-binding c) regulation of NR degradation. The capacity of the cell to utilize ammonium depends on availability of carbon sceletons. Accordingly, photosynthesis controls nitrate reduction at all levels (a to c). These photosynthesis effects are no direct light effects, but reflect the export of reducing power and of metabolites from the chloroplasts. Indeed, CO2-deficiency in the light can mimick darkness, and photosynthesis can be mimicked by sugar feeding in the dark. NR mRNA synthesis requires nitrate, yet it ceases in spite of high tissue nitrate concentrations when sugar levels fall below a critical level. The NR phosphorylation state does not depend much on nitrate, yet it is high in the light or when sugars are fed in the dark. NR protein degradation is much higher in the dark then in the light, yet again it can be slowed by sugar feeding, probably via changing the NR phosphorylation state and 14-3-3-binding. How sugars or their derivatives act in each of these cases is not known in detail, although there are indications (some of which are presented) that sugar phosphates may be the actual triggers.