Arabidopsis MADS-box factor AGL16 is a negative regulator of plant response to salt stress by downregulating salt-responsive genes

• Published in: The New phytologist Vol. 232; no. 6; pp. 2418 - 2439
• Main Authors: Zhao, Ping-Xia, Zhang, Jing, Chen, Si-Yan, Wu, Jie, Xia, Jing-Qiu, Sun, Liang-Qi, Ma, Shi-Song, Xiang, Cheng-Bin
• Format: Journal Article
• Language: English
• Published: England Wiley 01.12.2021; Wiley Subscription Services, Inc
• Subjects: ABA signalling; Abiotic stress; Abscisic Acid; AGL16; Arabidopsis; Arabidopsis - genetics; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis thaliana; Down-regulation; Elongation; Environmental stress; Gene Expression Regulation, Plant; Genes; Genetic analysis; Germination; Germination - genetics; Homeostasis; MADS‐box; Mutants; Phenotypes; plant response; Plants, Genetically Modified - metabolism; primary root elongation; root growth; Salt Stress; Salts; Seed germination; Seedlings - metabolism; Stress response; Stress, Physiological - genetics; Transcription; transcription (genetics); Transcription factors; Transcriptomics; Arabidopsis thaliana; MADS-box; ABA signalling; primary root elongation; salt stress; seed germination; AGL16
• ISSN: 0028-646X; 1469-8137; 1469-8137
• DOI: 10.1111/nph.17760

• Sessile plants constantly experience environmental stresses in nature. They must have evolved effective mechanisms to balance growth with stress response. Here we report the MADS-box transcription factor AGL16 acting as a negative regulator in stress response in Arabidopsis. • Loss-of-AGL16 confers resistance to salt stress in seed germination, root elongation and soil-grown plants, while elevated AGL16 expression confers the opposite phenotypes compared with wild-type. However, the sensitivity to abscisic acid (ABA) in seed germination is inversely correlated with AGL16 expression levels. • Transcriptomic comparison revealed that the improved salt resistance of agl16 mutants was largely attributed to enhanced expression of stress-responsive transcriptional factors and the genes involved in ABA signalling and ion homeostasis. We further demonstrated that AGL16 directly binds to the CArG motifs in the promoter of HKT1;1, HsfA6a and MYB102 and represses their expression. Genetic analyses with double mutants also support that HsfA6a and MYB102 are target genes of AGL16. • Taken together, our results show that AGL16 acts as a negative regulator transcriptionally suppressing key components in the stress response and may play a role in balancing stress response with growth.