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Turkish Journal of Botany

Abstract

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.

Author ORCID Identifier

DOĞA SELİN KAYIHAN: 0000-0002-7370-1575

DOI

10.55730/1300-008X.2891

Keywords

anthocyanin

First Page

134

Last Page

151

Publisher

The Scientific and Technological Research Council of Türkiye (TÜBİTAK)

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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