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.
Authors
- Liu Kai (ORCID: https://orcid.org/0000-0001-8569-6948)
- Huiping Chen (ORCID: https://orcid.org/0000-0002-0227-9100)
- Muhammad Qadir (ORCID: https://orcid.org/0000-0001-9139-7274)
- Long Wang (ORCID: https://orcid.org/0000-0002-3424-8181)
Institutions
- Chongqing University (CN)
- Intelligent Health (United Kingdom) (GB)
- Hunan Agricultural University (CN)
Publication Details
- Journal
- PLANT PHYSIOLOGY
- Published
- 2026-08-28
- DOI
- https://doi.org/10.1093/plphys/kiag643
- Primary Topic
- Light effects on plants
- Type
- article
- Field-Weighted Citation Impact
- 0.00