Nitrate is a nutrient signal that triggers complex regulation of transcriptional networks to modulate nutrient-dependent growth and development in plants. This includes time- and nitrate concentration-dependent regulation of nitrate-related gene expression. However, the underlying mechanisms remain poorly understood. Here we identify NIGT1 transcriptional repressors as negative regulators of the Arabidopsis NRT2.1 nitrate transporter gene, and show antagonistic regulation by NLP primary transcription factors for nitrate signalling and the NLP-NIGT1 transcriptional cascade-mediated repression. This antagonistic regulation provides a resolution to the complexity of nitrate-induced transcriptional regulations. Genome-wide analysis reveals that this mechanism is applicable to NRT2.1 and other genes involved in nitrate assimilation, hormone biosynthesis and transcription. Furthermore, the PHR1 master regulator of the phosphorus-starvation response also directly promotes expression of NIGT1 family genes, leading to reductions in nitrate uptake. NIGT1 repressors thus act in two transcriptional cascades, forming a direct link between phosphorus and nitrogen nutritional regulation.

Nitrogen is the most important macronutrient in plants and its supply induces responses in gene expression, metabolism and developmental processes. However, the molecular mechanisms underlying the nitrogen responses remain poorly understood. Here we show that the supply of nitrate but not ammonium immediately induces the expression of a transcriptional repressor gene in rice, designated NIGT1 (Nitrate-Inducible, GARP-type Transcriptional Repressor 1). The results of DNA-binding site selection experiments and electrophoretic mobility shift assays indicated that NIGT1 binds to DNA containing either of two consensus sequences, GAATC or GAATATTC. In transient reporter assays, NIGT1 was found to repress transcription from the promoters containing the identified NIGT1-binding sequences in vivo. Furthermore, NIGT1 repressed the activity of its own promoter, suggesting an autorepression mechanism. Consistently, nitrate-induced NIGT1 expression was found to be down-regulated after a transient peak during nitrate treatment, and the nitrate-induced expression of NIGT1 decreased in transgenic rice plants in which this gene was constitutively overexpressed. Furthermore, the chlorophyll content that could be a marker of nitrogen utilization was found to be decreased in NIGT1 overexpressors of rice grown with nitrate medium but not with ammonium medium. Thus, we propose NIGT1 as a nitrate-inducible and autorepressible transcriptional repressor that may play a role in the nitrogen response in rice. Taken together with the fact that the NIGT1-binding sites are conserved in promoter sequences of Arabidopsis NIGT1 homologs, our findings imply the presence of a time-dependent complex system for nitrate-responsive transcriptional regulation that is conserved in both monocots and dicots.

After the accident of the Fukushima 1 Nuclear Power Plant in March 2011, radioactive cesium was released and paddy fields in a wide area including Fukushima Prefecture were contaminated. To estimate the levels of radioactive Cs accumulation in rice produced in Fukushima, it is crucial to obtain the actual data of Cs accumulation levels in rice plants grown in the actual paddy field in Fukushima City. We herein conducted a two-year survey in 2011 and 2012 of radioactive and non-radioactive Cs accumulation in rice using a number of rice cultivars grown in the paddy field in Fukushima City. Our study demonstrated a substantial variation in Cs accumulation levels among the cultivars of rice.

The value of the T3 suppressed 20-min uptake test for the prediction of post-treatment outcome was studied in 193 unselected patients with Graves' disease treated with thionamide drugs and T3. One hundred and twenty-nine of 193 patients were studied previously and followed thereafter (Group A). Sixty-four were newly treated patients: thirty-three (Group B) were treated at the same hospital as Group A; thirty-one (Group C) were treated at another hospital. In total 126 patients out of 193 satisfied our criteria for suppression (total suppression rate, 65%). The suppression rate for new patients (55% in Group B, 52% in Group C) was similar to that for Group A in 1977 (49%) after comparable duration of treatment. The suppression rate for Group A increased with prolongation of the treatment period (49% in 1977 and 71% in 1981). As to the time course of suppression, it was observed that about two-thirds of the suppressed patients satisfied the criteria for suppression within 3 years of starting treatment. The number of suppressed patients per year decreased thereafter as the treatment periods increased. However, the yearly suppression rate did not decrease with time. The time course of suppression in each patient could not be predicted from the results of initial thyroid function tests. The overall remission rate among the 120 suppressed patients followed for 1-13 (mean, 4) years was 96%, which was almost equal to the value obtained in Group A in 1977 (95%) with the average follow-up period of 2 years. Among the 46 patients in Group A followed for 5-13 (mean, 7) years, no increase in relapse was observed with prolonged follow-up periods. Examination on the relationship between the duration of treatment and the post-treatment outcome revealed that, as a whole, the duration of treatment for the patients with relapse were rather short as compared with those for the patients in remission. These results confirm the usefulness of our T3 suppression test for predicting sustained remission of Graves' disease after treatment, and clearly indicate that long-term medical therapy could increase the number of remissions in patients with Graves' disease.