CHPO coordinates chilling recovery and nitrogen use in rice.
basic_science · Level V
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- Record sourced from PubMed, PMID 42310462.
- Also identified by DOI 10.1038/s41586-026-10682-6.
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Abstract
Global rice production faces mounting challenges from abnormal temperature fluctuations and nitrogen-fertilizer-driven environmental pollution<sup>1-7</sup>. Developing varieties that balance chilling resilience and nitrogen-use efficiency (NUE) offers a promising solution, but the molecular networks coordinating these traits remain poorly understood. Here we identify CHILLING PHOENIX (CHPO), a major gene underlying the quantitative trait locus shared by both chilling tolerance and resilience. It encodes a MYB transcription factor that acts as a key regulator coordinating post-chilling recovery with nitrogen use in rice. Natural variation in a GCG-repeat-encoded polyalanine tract alters CHPO DNA-binding preference and redirects regulatory outputs between the japonica-type (CHPO<sup>jap</sup>) and indica-type (CHPO<sup>ind</sup>), causing opposing effects on chilling tolerance and resilience. This allelic variation is shaped by domestication selection, with the CHPO<sup>jap</sup> allele probably derived from Chinese wild rice. CHPO<sup>jap</sup> directly targets OsTCP19 and OsNRT2.4 to fine-tune NUE, thereby enhancing chilling tolerance and resilience. These findings provide a mechanistic framework for a chilling-induced high-nitrogen-utilization module that alleviates the damage caused by chilling stress, and a potential molecular design strategy for breeding rice varieties with both chilling resilience and high NUE at the recovery stage.