Antagonistic regulation of nitrogen and drought signaling mediated by NIN-like protein 7 transcription factor in Arabidopsis thaliana
Abstract
Plants face the constant challenge of reconciling antagonistic environmental signals, such as nutrient-driven growth and water deficit-induced stress responses. However, the molecular mechanisms that integrate these conflicting pathways remain poorly understood. Through a comprehensive transcriptomic meta-analysis in Arabidopsis thaliana, we show that nitrogen (N) supply and water deficit signaling exhibit overlapping and often opposing gene expression responses. Regulatory network modeling identifies the NIN-LIKE PROTEIN 7 (NLP7) transcription factor (TF) as a central integrator of these convergent transcriptional responses. Through combinatorial water deficit and N supply treatments in wild-type and nlp7 mutant plants, we find that NLP7 accounts for 85% of the transcriptional interaction between these pathways. Chromatin immunoprecipitation and sequencing and a cell TF assay to detect TF regulation genome-wide reveal that NLP7 directly downregulate the expression of TFs such as HB6, NAC6, NAP, and WRKY18, which are central regulators of water deficit-mediated stress signaling. Repression of these secondary TFs has distinct downstream effects on gene expression, influencing shared and water deficit-specific responses. Loss of NLP7 enhances water deficit tolerance, characterized by increased water retention, reduced abscisic acid-mediated stomatal aperture, and altered expression of stress-responsive genes. These findings establish NLP7 as a central hub balancing growth and stress responses, providing insight into how plants integrate competing environmental cues.
Más información
| Título según WOS: | ID WOS:001676283100001 Not found in local WOS DB |
| Título de la Revista: | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA |
| Volumen: | 123 |
| Número: | 1 |
| Editorial: | NATL ACAD SCIENCES |
| Fecha de publicación: | 2026 |
| DOI: |
10.1073/pnas.2509904122 |
| Notas: | ISI |