Regulation of nitrate reductase transcript levels by glutamine accumulating in the leaves of a ferredoxin-dependent glutamate synthase-deficient gluS mutant of Arabidopsis thaliana, and by glutamine provided via the roots

The regulation by glutamine of the leaf transcript level corresponding to the Arabidopsis thaliana (L.) Heynh. nitrate reductase gene nia2 was examined using a novel approach: we took advantage of the ability of a ferredoxin-dependent glutamate synthase-deficient gluS mutant of A. thaliana to accumulate glutamine in the leaves when illuminated under conditions that favour photorespiration. The accumulation of glutamine in gluS mutant leaves and the concomitant decline in the leaf glutamate pool were not correlated with a reduction in the foliar nia2 transcript level. This result indicates that glutamine may not exert a negative control of the leaf nia2 transcript pool. The pattern of diurnal nia2 mRNA oscillation did not change upon illumination of the gluS mutant in air, although the leaf glutamine level remained high during the diurnal cycle. The amplitude of the diurnal fluctuation in nia2 transcript abundance, therefore, does not seem to depend on the size of the leaf glutamine pool (which normally fluctuates in opposite phase). This result also appears to argue against a role of glutamine as an effective repressor of nia2 transcript accumulation. The application of a solution containing 100 mM glutamine to the roots of A. thaliana resulted in an increase in the leaf glutamine level and in a decrease in the leaf nia2 transcript level. Net CO2 uptake and chlorophyll fluorescence quenching by attached leaves of A. thaliana were determined as a control of the physiological status of the plants and remained unaffected by the glutamine treatment. However, there was a decrease in the foliar nitrate level. The negative effect on the nia2 transcript pool exerted by exogeneous glutamine may, therefore, be explained as a result of the down-regulation of nitrate-uptake permeases in the roots by glutamine.