GASA13 and GASA14 mediate nitric oxide‑induced partial gibberellin insensitivity in Arabidopsis hypocotyl elongation.

Nitric oxide (NO) and gibberellin (GA) antagonistically regulate plant cell elongation. Here, we report an unexpected observation that NO confers partial GA-insensitivity on hypocotyl elongation in Arabidopsis thaliana. We identify GASA13 and GASA14 as essential downstream specificity filters underlying this phenomenon. Loss-of-function of GASA13 or GASA14 converted the NO-mediated inhibition from a partially GA-insensitive state to a fully GA-reversible state, as revealed by hypocotyl phenotyping analyses. Both GASA proteins showed increased protein accumulation upon NO treatment and decreased accumulation upon GA treatment, while their transcript levels were also regulated by DELLA. Hormone profiling showed that NO modulated bioactive GA levels in a GASA-dependent manner. Transcriptomic analysis revealed that wild-type plants exhibited a focused NO response, whereas gasa13 and gasa14 mutants displayed broad, diffuse transcriptional signatures, indicating a loss of signal specificity. Further analysis of GA metabolic and cell wall-related genes supported the model that GASA13 and GASA14 restrict NO-induced transcriptional changes to a precise growth-suppressive program. We propose that GASA13 and GASA14 act as downstream transcriptional specificity filters that channel NO signals into a focused output, conferring partial GA-insensitivity. This work uncovers a novel regulatory layer of NO-GA crosstalk beyond DELLA stabilization, and provides a mechanistic framework for understanding how plants achieve signal specificity during growth regulation.