Disruption of <i>ABI4</i> Enhances Anthocyanin Accumulation in <i>Arabidopsis</i> Seedlings Through HY5-Mediated Light Signaling

The AP2/ERF transcription factor ABSCISIC ACID INSENSITIVE 4 (ABI4) plays diverse roles in plant development and responses to abiotic stress. However, its potential involvement in regulating anthocyanin biosynthesis is not fully understood. In this study, three different loss-of-function <i>ab...

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Main Authors: Mingyang Zeng, Yan Wu, Shunfa Lin, Fang Zhang, Haiyan Jiang, Lixia Ma, Dong Liu
Format: Article
Language:English
Published: MDPI AG 2025-06-01
Series:Plants
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Online Access:https://www.mdpi.com/2223-7747/14/13/1905
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Summary:The AP2/ERF transcription factor ABSCISIC ACID INSENSITIVE 4 (ABI4) plays diverse roles in plant development and responses to abiotic stress. However, its potential involvement in regulating anthocyanin biosynthesis is not fully understood. In this study, three different loss-of-function <i>abi4</i> alleles (<i>abi4-1</i>, <i>abi4-2</i>, and <i>abi4-101</i>) were employed to investigate the role of ABI4 in the regulation of anthocyanin accumulation in <i>Arabidopsis</i> seedlings. These <i>abi4</i> mutants exhibited significantly increased anthocyanin accumulation, which was associated with elevated expression of genes involved in anthocyanin biosynthesis. HY5 (LONG HYPOCOTYL 5), a central component of photomorphogenesis, acts as a key light-regulated molecular switch. Further analysis revealed that ABI4 requires HY5 to function as a negative regulator of anthocyanin biosynthesis. Additionally, loss of <i>ABI4</i> resulted in heightened light sensitivity, leading to increased light-induced chlorophyll accumulation and chloroplast development, along with upregulation of photosynthesis-related genes. Interestingly, the light-hypersensitive phenotype of <i>abi4</i> mutants was partially rescued by the loss of HY5 function. Taken together, these findings demonstrate that <i>ABI4</i> negatively regulates anthocyanin accumulation in <i>Arabidopsis</i> seedlings through a HY5-dependent light signaling pathway.
ISSN:2223-7747