Global Transcriptomic Insights into NLA-Dependent Boron Toxicity Responses in Arabidopsis thaliana

Boron (B) toxicity disrupts multiple metabolic and signaling processes in plants, yet its interaction with post-translational regulators remains poorly understood. The E3 ubiquitin ligase NITROGEN LIMITATION ADAPTATION (NLA) is known to control nutrient transporter turnover, but its role in B toxicity responses has not been previously characterized. Here, we present the first genome-wide transcriptomic analysis of nla mutant Arabidopsis thaliana exposed to mild (1 mM) and moderate (2 mM) B toxicity. Loss of NLA caused a profound reprogramming of gene expression, marked by constitutive activation of ribosome- and translation-related pathways and strong repression of MAPK signaling, α-linolenic acid metabolism, and glucosinolate biosynthesis. Physiologically, nla mutants were unable to induce anthocyanin accumulation under toxic B conditions and instead redirected the phenylpropanoid pathway toward lignin biosynthesis. This shift coincided with the upregulation of circadian regulators (CCA1, LHY, HY5) and the downregulation of WRKY- and ERF-type transcription factors, suggesting that NLA is required for maintaining the circadian/phenylpropanoid regulatory balance necessary for anthocyanin induction. Together, our findings identify NLA as a previously unrecognized integrator of circadian, hormonal, and phenylpropanoid networks under B toxicity, and provide a set of candidate genes and pathways for improving B stress tolerance in plants.