CHROMATIN REMODELING FACTOR 28 and HEAT SHOCK FACTOR A2 activate BINDING IMMUNOGLOBULIN PROTEIN 3 under heat stress.

Abstract

Heat stress and the resulting endoplasmic reticulum (ER) stress pose substantial threats to plant growth and development. Our previous study revealed the heat-induced transcription of binding immunoglobulin protein 3 (CaBiP3), an ER-located heat shock protein from pepper (Capsicum annuum L.). However, the underlying regulatory mechanism remains unclear. This study reports that BiP3 enhances plant heat tolerance through increasing chlorophyll content, reducing ROS accumulation and relative electrolyte leakage, enhancing the upregulation of heat stress defensive genes, and mitigating ER stress in pepper and tomato (Solanum lycopersicum L.) plants. Furthermore, we identified two upstream regulators of CaBiP3, chromatin remodeling factor 28 (CaCHR28) and heat shock transcription factor A2 (CaHsfA2), that directly bind to the promoter of CaBiP3 and upregulate its expression to enhance plant heat tolerance. CaCHR28 also upregulates the expression of CaHsfA2, and heat stress enhances both proteins' activities in promoting the expression of CaBiP3. In summary, we have identified a conserved regulatory mechanism in plants in which CaCHR28 positively regulates plant heat tolerance by activating the transcription of CaBiP3 through CaHsfA2-dependent and -independent pathways.