A HAT1‐DELLA signaling module regulates trichome initiation and leaf growth by achieving GA homeostasis

Trichome initiation and leaf growth are two critical developmental processes in the plant life cycle, which need to be optimized in accordance with developmental stages and immediate surroundings. To a large extent, this optimization is achieved by fine-tuning of hormonal pathways, including the Gibberellins (GAs) pathway. However, the mechanism by which plants control GA homeostasis to optimize these two developmental processes is unknown. Here, we report HAT1, an HD-ZIP II transcriptional factor, negatively regulates the GA-mediated trichome initiation and cotyledon expansion. Both the transcript and protein levels of HAT1 are induced by GA, while increased HAT1, in return, suppresses GA biosynthesis and signaling, thus forming a negative feedback regulatory loop that controls GA homeostasis to fine-tune trichome development and cotyledon expansion. We also find that HAT1 interacts with DELLAs, including GAI and RGA. GAI inhibits both the protein stability and the binding activity of HAT1 regarding to its target genes. Overexpression of HAT1 in della5 can totally suppress the enhanced trichome initiation and enlarged cotyledon of della5. Our findings demonstrate that HAT1 functions as a critical repressor to regulate the GA-mediated trichome initiation and cotyledon growth; meanwhile they uncover a novel mechanism by which the plant regulates trichome initiation and cotyledon expansion through HAT1-DELLA regulatory module under various GA concentrations.