The indica and japonica rice (Oryza sativa) subspecies differ in nitrate (NO3−) assimilation capacity and nitrogen (N) use efficiency (NUE). Here, we show that a major component of this difference is conferred by allelic variation at OsNR2, a gene encoding a NADH/NADPH-dependent NO3− reductase (NR). Selection-driven allelic divergence has resulted in variant indica and japonica OsNR2 alleles encoding structurally distinct OsNR2 proteins, with indica OsNR2 exhibiting greater NR activity. Indica OsNR2 also promotes NO3− uptake via feed-forward interaction with OsNRT1.1B, a gene encoding a NO3− uptake transporter. These properties enable indica OsNR2 to confer increased effective tiller number, grain yield and NUE on japonica rice, effects enhanced by interaction with an additionally introgressed indica OsNRT1.1B allele. In consequence, indica OsNR2 provides an important breeding resource for the sustainable increases in japonica rice yields necessary for future global food security.

Summary Understanding the genetic basis of natural variation in grain size among diverse rice varieties can help breeders develop high‐yielding rice cultivars. Here, we report the discovery of qTGW2, a new semidominant quantitative trait locus for grain width and weight. The corresponding gene, TGW2, encodes CELL NUMBER REGULATOR 1 (OsCNR1) localized to the plasma membrane. A single nucleotide polymorphism (SNP) variation 1818 bp upstream of TGW2 is responsible for its different expression, leading to alteration in grain width and weight by influencing cell proliferation and expansion in glumes. TGW2 interacts with KRP1, a regulator of cell cycle in plants, to negatively regulate grain width and weight. Genetic diversity analysis of TGW2 in 141 rice accessions revealed it as a breeding target in a selective sweep region. Our findings provide new insights into the genetic mechanism underlying grain morphology and grain weight, and uncover a promising gene for improving rice yield.

Summary ATP ‐citrate lyases ( ACL ) play critical roles in tumour cell propagation, foetal development and growth, and histone acetylation in human and animals. Here, we report a novel function of ACL in cell death‐mediated pathogen defence responses in rice. Using ethyl methanesulphonate ( EMS ) mutagenesis and map‐based cloning, we identified an Oryza sativa ACL ‐A2 mutant allele, termed spotted leaf 30‐1 ( spl30‐1 ), in which an A‐to‐T transversion converts an Asn at position 343 to a Tyr (N343Y), causing a recessive mutation that led to a lesion mimic phenotype. Compared to wild‐type plants, spl30‐1 significantly reduces ACL enzymatic activity, accumulates high reactive oxygen species and increases degradation rate of nuclear deoxyribonucleic acids. CRISPR /Cas9‐mediated insertion/deletion mutation analysis and complementation assay confirmed that the phenotype of spl30‐1 resulted from the defective function of Os ACL ‐A2 protein. We further biochemically identified that the N343Y mutation caused a significant degradation of SPL 30 N343Y in a ubiquitin‐26S proteasome system ( UPS )‐dependent manner without alteration in transcripts of Os ACL ‐A2 in spl30‐1 . Transcriptome analysis identified a number of up‐regulated genes associated with pathogen defence responses in recessive mutants of Os ACL ‐A2, implying its role in innate immunity. Suppressor mutant screen suggested that Os SL , which encodes a P450 monooxygenase protein, acted as a downstream key regulator in spl30‐1 ‐mediated pathogen defence responses. Taken together, our study discovered a novel role of Os ACL ‐A2 in negatively regulating innate immune responses in rice.

Lesion-mimic mutants (LMMs) provide a valuable tool to reveal the molecular mechanisms determining programmed cell death (PCD) in plants. Despite intensive research, the mechanisms behind PCD and the formation of lesions in various LMMs still remain to be elucidated. Here, we identified a rice (Oryza sativa) LMM, early lesion leaf 1 (ell1), cloned the causal gene by map-based cloning, and verified this by complementation. ELL1 encodes a cytochrome P450 monooxygenase, and the ELL1 protein was located in the endoplasmic reticulum. The ell1 mutant exhibited decreased chlorophyll contents, serious chloroplast degradation, upregulated expression of chloroplast degradation-related genes, and attenuated photosynthetic protein activity, indicating that ELL1 is involved in chloroplast development. RNA sequencing analysis showed that genes related to oxygen binding were differentially expressed in ell1 and wild-type plants; histochemistry and paraffin sectioning results indicated that hydrogen peroxide (H 2 O 2) and callose accumulated in the ell1 leaves, and the cell structure around the lesions was severely damaged, which indicated that reactive oxygen species (ROS) accumulated and cell death occurred in the mutant. TUNEL staining and comet experiments revealed that severe DNA degradation and abnormal PCD occurred in the ell1 mutants, which implied that excessive ROS accumulation may induce DNA damage and ROS-mediated cell death in the mutant. Additionally, lesion initiation in the ell1 mutant was light dependent and temperature sensitive. Our findings revealed that ELL1 affects chloroplast development or function, and that loss of ELL1 function induces ROS accumulation and lesion formation in rice.