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PubMed · 42363596

From activation to desensitization: How ABA balances plant growth and abiotic stress response?

Abstract

Abscisic acid (ABA) signaling is a central regulator of plant adaptation to abiotic stress, dynamically coordinating stress responses with growth and development. Rapid activation of ABA signaling promotes plant survival during the early stages of stress, whereas prolonged stress requires timely attenuation of the pathway to restore growth and prevent excessive stress responses. Recent studies have uncovered diverse mechanisms underlying ABA desensitization, including regulation of SnRK2 kinases, phytohormone crosstalk, nutrient signaling, protein trafficking, post-translational modifications, and feedback regulatory networks. Together, these interconnected mechanisms enable plants to fine-tune ABA signaling in response to developmental and environmental cues. In this review, we summarize recent advances in understanding the molecular mechanisms that attenuate ABA signaling and restore the balance between growth and stress adaptation during prolonged stress. We also highlight outstanding questions and discuss strategies for engineering ABA signaling dynamics to improve crop resilience, productivity, and adaptation to increasingly variable environments.

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BibTeXRIS

Wenguan Zhou, Yueni Fan, Weiqiang Li, Lam-Son Phan Tran, Kai Shu. 2026-06-26. From activation to desensitization: How ABA balances plant growth and abiotic stress response?. https://doi.org/10.1016/j.xplc.2026.101977

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Ultraviolet-B-induced OsKOL4 promotes ABA accumulation by inhibiting OsABA8ox1 and OsABA8ox2 expression.

Ultraviolet-B (UV-B) light is a component of sunlight that influences plant survival and adaptation. UV-B induces plants to regulate their phenotypes and metabolism to increase resistance to UV-B and associated stresses. Abscisic acid (ABA) metabolism and signaling are important for plant responses to UV-B. However, the mechanisms underlying UV-B-induced ABA accumulation and signaling in rice remain poorly understood. Here, we report that ENT-KAURENE OXIDASE LIKE 4 (OsKOL4) regulates UV-B-induced responses and ABA biosynthesis. UV-B activates OsKOL4 expression via OsbZIP48, an ELONGATED HYPOCOTYL 5 (HY5) homolog that directly binds to the OsKOL4 promoter. Rice plants overexpressing OsKOL4 exhibit UV-B-induced phenotypes under normal conditions, along with ABA overaccumulation phenotypes resulting from increased ABA levels. Moreover, UV-B promotes ABA accumulation by inhibiting the expression of the ABA 8'-HYDROXYLASE1 and ABA 8'-HYDROXYLASE 2 (OsABA8ox1/2) genes through OsKOL4. OsKOL4 interacts with the transcription factor AP2/ERF ON CHROMOSOME 3 (OsAPE3), which in turn represses the transcription of OsABA8ox1/2. Furthermore, both UV-B and OsKOL4 enhance the binding of OsAPE3 to the OsABA8ox1/2 promoters. Collectively, our findings demonstrate that the OsKOL4-OsAPE3 module regulates ABA homeostasis in response to UV-B signaling by reducing ABA catabolism.

Abscisic Acid