The Chromatin Remodeler PEL1.2 Coordinates GA/JA Homoeostasis to Promote Panicle Exsertion for Hybrid Rice Seed Production

ABSTRACT Short panicle exsertion length (PEL) severely restricts outcrossing pollination efficiency and yield in hybrid rice seed production, yet the regulatory network coordinating chromatin architecture and hormonal homoeostasis underlying PEL remains elusive. Here, we report a hormone‐centred regulatory mechanism driven by chromatin remodelling that controls PEL. Through map‐based cloning, we identified the causal gene PEL1.2 , which encodes a Snf2‐family chromatin remodelling factor. Mechanistically, our results reveal that PEL1.2 functions by reshaping the chromatin landscape to modulate the transcription of target genes. In this model, PEL1.2 displaces nucleosomes to create an open chromatin state at the promoters of target genes, thereby facilitating the access of specific transcription factors to activate gene expression. This transcriptional regulation significantly elevates bioactive gibberellic acid 4 (GA 4 ) levels while antagonistically suppressing jasmonic acid accumulation, establishing a GA‐dominant hormonal homoeostasis that drives uppermost internode cell elongation. Furthermore, introgression of the elite PEL1.2 allele into sterile lines significantly alleviated panicle enclosure, thereby enhancing the outcrossing seed setting rate of the sterile lines and ultimately increasing the yield of hybrid F 1 seed production. These findings reveal a pivotal chromatin‐hormone module, providing a theoretical basis for improving hybrid rice seed production.