NITROGEN RESPONSE DEFICIENCY 1-mediated CHL1 induction contributes to optimized growth performance during altered nitrate availability in Arabidopsis.

Abstract

Plants cannot fix nitrogen directly; they must absorb it from the soil through their roots, or in rare cases, form associations with nitrogen-fixing bacteria. The efficiency of nitrogen use in most domesticated crops is low, and more than half of the available nitrogen in the soil can leach into the environment. Understanding the nitrogen signaling pathways is essential for maximizing the efficiency of nitrogen use in crops. In the present study, we characterized the Myeloblastosis (Myb)-like gene NITROGEN RESPONSE DEFICIENCY 1 (NID1). We observed that the growth performance of nid1 knockout (KO) mutant Arabidopsis plants was better than that of wild-type Col-0 plants under very low-nitrate conditions, leading to improved growth performance in the nid1 KO plants. The results of chromatin immunoprecipitation and electrophoretic mobility shift assays indicated that NID1 binds to the promoter of the NITRATE TRANSPORTER (NRT)1.1 gene. Furthermore, nid1 KO plants exhibited similar growth performance to the nid1 KO/chl1-5 (nrt1.1 KO) double mutant and chl1-5 (nrt1.1 KO) plants in response to low-nitrate conditions. We suggest that NID1 plays a crucial role as a transcription factor in optimizing plant growth by modulating the transcript abundance of the nitrate transceptor CHL1, leading to enhanced ABA accumulation in low-nitrate conditions.