Grain number per panicle critically determines rice yield. Although many underlying genes have been reported, yet the molecular mechanisms linking ethylene to panicle development remain unclear. Here, we identify GRAIN NUMBER PER PANICLE 3 (GNP3) as a regulator of GNP through genome-wide association study (GWAS) combined with map-based cloning. GNP3 encodes a MITOGEN-ACTIVATED PROTEIN KINASE KINASE KINASE 22 (OsMKKK22) that phosphorylates S-adenosyl-L-methionine synthetase 1 (SAMS1), triggering its degradation to suppress ethylene biosynthesis. Ethylene overaccumulation in gnp3-1 mutants reduces grain number, while GNP3 overexpression enhances panicle branching and grain yield by lowering ethylene levels. We demonstrate that a natural haplotype GNP3^Hap-Tprevalent in indica subspecies strengthens GNP3-SAMS1 interaction, accelerating SAMS1 degradation and improving grain number. Furthermore, overexpressing GNP3 increases grain yield by approximately 20% in field plot conditions. Our findings unveil a MAPK-ethylene regulatory module and highlight GNP3^Hap-T as a valuable genetic resource for breeding high-yield rice.

Grain size substantially influences rice quality and yield. In this study, we identified CONTROL OF SLENDER RICE 1 ( COR1 ), a quantitative trait locus encoding an F-box protein that enhances grain length by promoting cell proliferation. The transcription factor OsbZIP35 represses COR1 expression, while COR1 interacts with OsTCP19, leading to its degradation. Knockout of either OsbZIP35 or OsTCP19 results in increased grain length, confirming their regulatory roles in grain development. The OsbZIP35-COR1-OsTCP19 module controls the expression of the cell cycle gene OsCycB1;4 , thereby modulating cell proliferation and ultimately determining grain size. Five haplotypes of COR1 were identified, with COR1 -Hap1 and COR1 -Hap3 being elite alleles associated with longer grains. Field plot trials demonstrated that the near-isogenic line NIL- COR1 ^SLG increased yield by ~6.6% compared to NIL- COR1 ^Nip . These findings elucidate the genetic mechanisms underlying grain size regulation and offer promising strategies for improving rice yield.

Improving multistress resilience in crops is essential for sustainable agriculture, yet the genetic mechanisms coordinating abiotic and biotic stress responses remain poorly understood. This study identifies CTS1 ( Cold Tolerance at the Seedling stage1 ), encoding the transcription factor OsWRKY74, as a key pleiotropic regulator that mediates both cold tolerance and blast resistance in rice. Through genome-wide association study, we found that CTS1 negatively regulates cold tolerance at the seedling stage. The natural allele CTS1 ^Hap1 confers greater cold tolerance than CTS1 ^Hap2 by mildly repressing the expression of CTB2 , thereby maintaining sterol glycoside homeostasis and membrane stability. Furthermore, during Magnaporthe oryzae infection, CTS1 activates the expression of OsHSP90 and upregulates pathogenesis-related genes, thereby enhancing blast resistance. Our findings reveal a dual-function mechanism of CTS1 in stress adaptation and provide valuable alleles for breeding multistress resilient rice varieties.