Table IV.

Hypotheses concerning the regulation of IHATS expression and supporting observations

Hypothesis	Observation
NO3− is not responsible for down-regulating HvNRT2 transcript levels.	Tungstate treatment increased HvNRT2 transcript abundance (Figs. 3B and 4).
NO3− may act post-transcriptionally.	Tungstate treatment decreased NO3− influx (Fig. 3A).
Elevated concentrations of NH4+ down-regulate HvNRT2 transcript levels.	MSO decreased HvNRT2 transcript levels, when applied together with NH4+ (Table III).
NH4+ exerts post-transcriptional effects.	MSO was capable of reducing NO3− influx substantially without significantly affecting HvNRT2 transcript levels (Figs. 3, A and B, and 4).
Gln is the main down-regulator of HvNRT2 transcript levels.	NH4+ treatment dramatically decreased HvNRT2 transcript level when its conversion to Gln was not blocked by MSO (Table III).
	Addition of all amino acids increased root Gln levels, and decreased HvNRT2 transcript levels (Table I; Fig. 2B).
	When root Glu and Gln concentrations were increased by exogenous application, HvNRT2 transcript levels were inversely correlated with Glu and Gln concentrations.
	Tungstate treatment reduced root Gln by 81%, without affecting root Glu. This treatment produced a 20%–30% increase of HvNRT2 mRNA.
	Treatments with AZA decreased root [Glu] by 90%, increased root [Gln] by 43%, and decreased HvNRT2 transcript levels and 13NO3− by 97% and 95%, respectively (Table II; Fig. 3).