CmHSFA3-CmBRC1a-CmHB40 module inhibits axillary bud development in response to high temperature

Abstract

Branching is a key determinant of plant architecture, directly influencing growth, yield, and resource allocation. High temperature (HT) inhibits plant growth and development, often leading to alterations in plant architecture. However, the molecular mechanisms underlying temperature-induced inhibition of branching remain elusive. Here, we discovered that CmBRC1a is strongly induced by HT and inhibits axillary bud development in chrysanthemum. We further demonstrated that the heat shock transcription factor CmHSFA3 directly activates CmBRC1a by binding to its promoter, thus acting as its upstream regulator. Overexpression of CmHSFA3 further confirmed its role in suppressing branching. The finding that HT cannot completely suppress the enhanced branching phenotype of CmBRC1a knockdown lines suggests that HT-regulated branching is not entirely dependent on CmBRC1a. Similar to previously reported BRC1-mediated pathways, CmBRC1a directly activates the expression of CmHB40, thereby increasing abscisic acid (ABA) accumulation, which ultimately inhibits shoot branching. Our findings reveal CmHSFA3-CmBRC1a-CmHB40 module inhibits axillary bud development in response to HT, providing new insights into how environmental cues shape plant architecture.