BEL1-LIKE HOMEODOMAIN6 and KNOTTED ARABIDOPSIS THALIANA7 Interact and Regulate Secondary Cell Wall Formation via Repression of REVOLUTA

• Published in: The Plant cell Vol. 26; no. 12; pp. 4843 - 4861
• Main Authors: Liu, Yuanyuan, You, Shijun, Li, Wenhua L., Schuetz, Mathias, Brady, Siobhan M., Douglas, Carl J.
• Format: Journal Article
• Language: English
• Published: United States American Society of Plant Biologists 01.12.2014
• Subjects: Arabidopsis; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis - ultrastructure; Arabidopsis Proteins - chemistry; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis Proteins - physiology; Arabidopsis thaliana; Binding Sites; Biosynthesis; Cell Wall - metabolism; Cell walls; Gene Expression Profiling; Gene expression regulation; Gene Expression Regulation, Plant; Homeodomain Proteins - chemistry; Homeodomain Proteins - genetics; Homeodomain Proteins - metabolism; Homeodomain Proteins - physiology; homeostasis; Inflorescences; Phenotype; Phenotypes; Plant cells; Plant Leaves - genetics; Plant Leaves - growth & development; Plant Leaves - metabolism; Plant Leaves - ultrastructure; Plants; Plants, Genetically Modified - metabolism; Promoter Regions, Genetic; Protein Interaction Domains and Motifs; Proteins; Repressor Proteins - genetics; Repressor Proteins - metabolism; Repressor Proteins - physiology; rev genes; Transcription factors
• ISSN: 1040-4651; 1532-298X; 1532-298X
• DOI: 10.1105/tpc.114.128322

The TALE homeodomain transcription factor KNOTTED ARABIDOPSIS THALIANA7 (KNAT7) is part of a regulatory network governing the commitment to secondary cell wall biosynthesis of Arabidopsis thaliana, where it contributes to negative regulation of this process. Here, we report that BLH6, a BELLI-LIKE HOMEODOMAIN protein, specifically interacts with KNAT7, and this interaction influences secondary cell wall development. BLH6 is a transcriptional repressor, and BLH6-KNAT7 physical interaction enhances KNAT7 and BLH6 repression activities. The overlapping expression patterns of BLH6 and KNAT7 and phenotypes of blh6, knat7, and blh6 knat7 loss-of-function mutants are consistent with the existence of a BLH6-KNAT7 heterodimer that represses commitment to secondary cell wall biosynthesis in interfascicular fibers. BLH6 and KNAT7 overexpression results in thinner interfascicular fiber secondary cell walls, phenotypes that are dependent on the interacting partner. A major impact of the loss of BLH6 and KNAT7 function is enhanced expression of the homeodomainleucine zipper transcription factor REVOLUTA/INTERFASCICULAR FIBERLESS1 (REV/IFL1). BLH6 and KNAT7 bind to REV promoter and repress REV expression, while blh6 and knat7 interfascicular fiber secondary cell wall phenotypes are suppressed in blh6 rev and knat7 rev double mutants, suggesting that BLH6/KNAT7 signaling acts through REV as a direct target.