The 14-3-3 proteins, a highly conserved class in all eukaryotes, are widely associated with plant growth and stress responses. However, their role in plant immunity and its regulatory mechanisms remains elusive. Here, we show that two homologous rice 14-3-3 proteins, OsGF14f and OsGF14c, function redundantly to enhance rice resistance against Magnaporthe oryzae. The E3 ligase OsPUB20 targets OsGF14f and OsGF14c for ubiquitination and 26S proteasome-mediated degradation, thereby negatively regulating rice immunity. Remarkably, chitin perception activates the receptor-like cytoplasmic kinase OsRLCK185 that phosphorylates OsPUB20 at Thr153, which stabilizes OsGF14f and enhances rice blast resistance. Furthermore, during M. oryzae infection, OsGF14f translocates into the nucleus, where it facilitates the degradation of OsWRKY42, a transcription factor that negatively regulates defense responses. Collectively, our findings reveal a phosphorylation-dependent ubiquitination switch that links cell surface chitin perception to nuclear immune reprogramming during M. oryzae invasion.

Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors play a critical role in plant defense, but the mechanisms regulating their expression remain incompletely understood. Here, we report that the rice CCCH-tandem zinc-finger protein OsTZF1 interacts with both AvrPiz-t interacting protein 10 (APIP10) and the NLR protein Piz-t. OsTZF1 positively regulates rice immunity by increasing the transcript levels of OsSGT1 and OsKS4 through binding to the AAAGC motif. However, in Piz-t-carrying plants, knockout of OsTZF1 results in increased Piz-t transcript and protein levels, thus enhancing resistance to virulent strains of Magnaporthe oryzae without a growth penalty. Furthermore, we demonstrate that OsTZF1 can directly bind to the AAAGC motif of Piz-t, thereby repressing its expression level. Thus, OsTZF1 functions as a dual regulator: it activates general defense genes while suppressing Piz-t-mediated resistance to virulent strains, balancing resistance and growth. These findings reveal a strategy for engineering NLR-mediated resistance in crops by fine-tuning immune regulators to achieve both disease resistance and yield stability.

Small G proteins, functioning as monomeric GTPases, are critical molecular switches that regulate diverse processes in plants. However, little is known about their protein homeostasis during immune responses. Here, we demonstrate that OsRab11C1, encoding a Rab-type GTPase, is transcriptionally upregulated upon Magnaporthe oryzae infection. Strikingly, loss of OsRab11C1 enhances rice blast resistance, concomitant with increased defense gene expression, MAPK activation, and ROS burst. Mechanistically, we identify the E3 ubiquitin ligase EL5 as an interactor that ubiquitinates and targets OsRab11C1 for degradation via the 26S proteasome. Consistently, EL5 acts upstream of OsRab11C1 and positively regulates rice immunity. Further analysis reveals that OsRab11C1 interacts with and stabilizes mitogen-activated protein kinase kinase OsMKK6, thereby facilitating its autophosphorylation activity. In return, OsMKK6 acts as a negative regulator of rice programmed cell death and immunity. Collectively, our findings unveil a dynamic EL5-OsRab11C1-OsMKK6 signaling module that orchestrates rice immunity against pathogen invasion.

The resistance of crops against diseases is constrained by the number of resistance genes. Recent studies revealed that the lectin receptor-like kinases (LecRLKs) function as novel pattern recognition receptors or trigger chloroplast ROS burst. Some LecRLK alleles confer resistance to multiple fungal diseases, demonstrating LecRLKs are emerging as immune hubs.

China has a long history of rice cultivation and a rich rice-farming culture. As the world’s largest producer and consumer of rice, continuously advancing rice research and production is vital to ensuring food security. In this review, we systematically summarize the progress in rice research and production over the past decade (2015–2025) and highlight emerging challenges in China. This review synthesizes national and regional characteristics of rice production, consumption, trade, along with advances in the conservation and utilization of rice germplasm resources, the molecular mechanisms of domestication and genomics. It provides an in-depth elaboration of the molecular and genetic basis governing rice agronomic traits, including yield components, grain quality, hybrid fertility, nutrient-use efficiency, and abiotic/biotic resistance. This is followed by a comprehensive overview of rice cultivar improvement adapted to the major ecological zones. This work further highlights the transformative shift in rice cultivation management from traditional labor-intensive farming to simplified, smart, and unmanned cultivation systems. Future directions for rice breeding are discussed, with a focus on the integration of molecular design, multi-omics, and artificial intelligence technologies to build high-efficiency breeding systems that are conducive to sustainable and resilient rice production in China.

Pathogens commonly secrete effectors into host cells to facilitate invasion. In the host ubiquitin-proteasome system (UPS), E3 ubiquitin ligases often target pathogen effectors for degradation, thereby enhancing immune responses. In turn, pathogen effectors frequently disrupt E3 ligase function to promote virulence. However, it remains largely unclear whether pathogen effectors also interfere with other enzymes of the UPS, such as E2 ubiquitin-conjugating enzymes. In this study, we identified a conserved effector, MoCE1, that is essential for the pathogenicity of Magnaporthe oryzae. MoCE1 is secreted into rice cells, where it interacts with the rice E3 ligase OsRING10 and the E2 enzyme OsUBC11. Upon M. oryzae infection, OsRING10 and OsUBC11 act synergistically to degrade MoCE1 through K48-linked polyubiquitination. Overexpression of either OsRING10 or OsUBC11 enhances resistance to M. oryzae. To counteract this defence, MoCE1 inhibits the enzymatic activity of OsUBC11. Collectively, these findings reveal a nuanced mechanism in which a pathogen effector, regulated by a host E2-E3 pair, disrupts E2 function to escape UPS-mediated immunity in plants.

Plant respiratory burst oxidase homologs (Rbohs) contribute to the production of reactive oxygen species, which are crucial defense signals in plants. However, the regulation of rice (Oryza sativa) OsRboh homeostasis has remained unclear. In this study, we reported that overexpression of OsRbohB confers resistance to Magnaporthe oryzae and Xanthomonas oryzae pv. oryzae. Mechanistically, the calcium-dependent protein kinase OsCPK4 interacts with and phosphorylates OsRbohB at Ser322 and Ser326, thereby reducing immune responses. OsRbohB phosphomimic modifications at these 2 sites disrupt OsRbohB-mediated disease resistance. Moreover, the RING-type E3 ubiquitin ligase OsRING142 interacts with and ubiquitinates OsRbohB at Lys266, targeting it for degradation by the 26S proteasome pathway and compromising the immune response. Overexpression of OsRbohBK266R further increased resistance compared with OsRbohB overexpression plants. Remarkably, phosphorylation at OsRbohB facilitates OsRING142-mediated ubiquitination and degradation of OsRbohB. OsRbohBK266R×S2A overexpression plants with reduced ubiquitination and phosphorylation levels of OsRbohB exhibit stronger resistance against M. oryzae. Overall, our study highlights the critical role of Rbohs in broad-spectrum resistance and demonstrates that phosphorylation and ubiquitination synergistically fine-tune Rboh protein stability and immunity.

Rice false smut, caused by the fungal pathogen Ustilaginoidea virens, is a devastating disease affecting major rice-growing regions. A new study reveals that exopolysaccharides secreted by rhizosphere Sphingomonadaceae bacteria break the dormancy of U. virens chlamydospores and facilitate root colonization.

Rice is a vital staple food that sustains half of the world's population. However, it is constantly under threat from a variety of pathogens, including at least 13 fungi, 5 bacteria, 8 viruses, and 6 nematodes. These pathogens can significantly reduce rice yields, posing a serious risk to global food security. The increasing frequency of extreme weather events, coupled with the effects of climate change, has further exacerbated the spread and mutation of these pathogens, leading to a decline in agricultural productivity. This review highlights the major diseases affecting rice in China, including three fungal diseases (rice blast, rice false smut, and rice sheath blight), two bacterial diseases (rice bacterial blight and bacterial leaf streak), two viral diseases (southern rice black‐streaked dwarf disease and rice stripe virus), and one nematode (rice root‐knot nematodes). The review also proposes future directions for an integrated approach to control these major rice diseases. Overall, addressing the threats posed by these pathogens is crucial to ensure a stable and secure global food supply.

The COP9 signalosome (CSN) is a highly conserved protein complex in eukaryotes, with CSN5 serving as its critical catalytic subunit. However, the role of CSN5 in plant immunity is largely unexplored. Here, we found that suppression of OsCSN5 in rice enhances resistance against the fungal pathogen Magnaporthe oryzae and the bacterial pathogen Xanthomonas oryzae pv. oryzae ( Xoo ) without affecting growth. OsCSN5 is ubiquitinated and degraded by the E3 ligase OsPUB45. Overexpression of OsPUB45 increased resistance against M. oryzae and Xoo , while dysfunction of OsPUB45 decreased resistance. In addition, OsCSN5 stabilized OsCUL3a to promote the degradation of a positive regulator OsNPR1. Overexpression of OsPUB45 compromised accumulation of OsCUL3a, leading to stabilization of OsNPR1, whereas mutations in OsPUB45 destabilized OsNPR1. These findings suggest that OsCSN5 stabilizes OsCUL3a to facilitate the degradation of OsNPR1, preventing its constitutive activation without infection. Conversely, OsPUB45 promotes the degradation of OsCSN5, contributing to immunity activation upon pathogen infection.

Plants are subject to attack by diverse pests and pathogens. Few genes conferring broad-spectrum resistance to both insects and pathogens have been identified. Because of the growth-defense tradeoff, it is often challenging to balance biotic stress resistance and yield for crops. Here, we report that OsWRKY36 suppresses the resistance to insects and pathogens via transcriptional repression of Phenylalanine Ammonia Lyases (PALs), a key enzyme in phenylpropanoid pathway in rice. Knocking out OsWRKY36 causes elevated lignin biosynthesis and increased sclerenchyma thickness of leaf sheath, leading to enhanced resistance to multiple pests and pathogens. Additionally, loss of OsWRKY36 also derepresses the transcription of Ideal Plant Architecture 1 (IPA1) and MONOCULM2 (MOC2), resulting in increased spikelet number per panicle and tiller number. These findings provide mechanistic insights into biotic stress tolerance in rice and offer a promising strategy to breed rice cultivars with broad-spectrum resistance to insects and pathogens while maintaining stable yield.

Broad-spectrum resistance (BSR) reduces pathogen-related yield losses in crops such as rice (Oryza sativa). To achieve BSR, traditional breeding has focused on the time-intensive process of incorporating resistance (R) genes into elite germplasm. Now, CRISPR/Cas9-mediated genome editing makes it possible to modify susceptibility (S) genes to rapidly achieve BSR in rice. However, identifying S genes remains challenging. Here, we analyzed transcriptome data and determined that OsJAC1, encoding a mannose-binding jacalin-related lectin, is significantly induced upon infection by the rice blast fungus Magnaporthe oryzae. To explore the role of OsJAC1 in BSR in rice, we generated OsJAC1 overexpression and knockout mutant lines in the rice ZH11 (Zhonghua 11) background and performed pathogen inoculation assays, revealing that OsJAC1 negatively regulates resistance against M. oryzae and the bacterial blight pathogen Xanthomonas oryzae pv. oryzae. Further evidence of defense responses, such as a reactive oxygen species burst, defense-related gene expression, and MAPK phosphorylation, also supports the role of OsJAC1 as a negative regulator of plant immunity. To further validate the function of OsJAC1, we knocked out OsJAC1 in the Nipponbare (NPB) background. The resulting NPB-osjac1cas9 plants showed enhanced defense responses and resistance against M. oryzae. Notably, the osjac1 mutants did not compromise agronomic traits in the ZH11 or NPB background. Hence, OsJAC1 could be regarded as an S gene and could serve as a potential target in rice breeding programs, providing valuable insights for crop improvement.

>Immune-related receptor-like kinases(RLKs) and receptor-like cytoplasmic kinases(RLCKs) enable plant cells to rapidly transduce and amplify immune signals at an early stage of pathogen attack, which is essential for plant survival, and these immune kinases must be tightly controlled to prevent aberrant activation. The U-box type E3 ubiquitin ligase SPL11(Os PUB11) has been shown to trigger the ubiquitination and degradation of the S-locus RLK SDS2 to attenuate immunity in rice.

ROP GTPases regulate various cellular processes, including plant immunity. While ROP GTPase activation has been reported during plant immune responses, the mechanisms underlying the dynamic deactivation of ROP GTPases remain unclear. In this study, we identified the autophagy kinase OsATG1 as a key regulator that interacts with and phosphorylates SPIN6, a plant-specific ROP GTPase-activating protein (RhoGAP), which in turn deactivates the ROP GTPase OsRac1. OsATG1-mediated multi-site phosphorylation is necessary for the GAP activity of SPIN6 to hydrolyze OsRac1-GTP, and overexpression of a phosphomimic form of SPIN6 attenuates rice immunity. We showed that two isoforms of OsATG1, OsATG1a and OsATG1b, operate redundantly in rice immunity to the fungal pathogen Magnaporthe oryzae. Double mutants of OsATG1a and OsATG1b exhibit stronger resistance as well as developmental defects and complete sterility. Moreover, OsATG1 interacts with OsATG8. Phenotypic analyses of OsATG8 transgenic plants reveal that OsATG8 positively regulates rice immunity, but OsATG8 activates immunity partially independent of its function in autophagy, because overexpressing the lipidation-defective OsATG8G117A or accumulating non-lipidated OsATG8 in the osatg7 mutant enhances rice disease resistance. Mechanistically, OsATG8 promotes OsATG1 turnover, whereas OsATG8G117A is sufficient to deplete OsATG1, leading to SPIN6 dissociation and degradation. As autophagy is essential in nutrient recycling, we found that nutrient limitations induce OsATG8 expression and rice immunity while suppressing SPIN6. However, SPIN6 phosphorylation inhibits this nutrient-limitation-induced immunity. Taken together, our results suggest that OsATG1 and OsATG8 possess autophagy-independent functions to transform nutrient limitation into immunity via plant-specific ROP GTPase signaling.

The mechanisms underlying virus perception and immune activation in plants remain poorly understood. Recent work shows that in rice, an E3 ubiquitin ligase senses viral coat proteins to activate the jasmonate signalling pathway by degrading NINJA3, and triggers downstream antiviral defence responses.

Knocking out three susceptibility genes (Pi21, Bsr-d1, and Xa5) in a rice breeding line that contains the resistance Piz-t produced enhanced broad-spectrum resistance against the fungal pathogen Magnaporthe oryzae and the bacterial pathogen Xanthomonas oryzae pv. oryzae without obvious growth penalty.

In crop plants, there is often a trade-off between growth and defense; modulating the balance is crucial for effective crop improvement. In rice (Oryza sativa), the DENSE AND ERECT PANICLE 2 (DEP2) mutant shows altered phenotypes such as a more vertical leaf angle, erect panicles, small and round grains, slightly lower thousand-grain weight, and dwarfism. Here, we determined that loss of DEP2 function enhances resistance to the rice blast fungus Magnaporthe oryzae. We established that DEP2 interacts with the E3 ubiquitin ligase OsRING80, which ubiquitinates DEP2 and promotes its degradation via the 26S proteasome pathway. Interestingly, the transcriptional level of OsRING80 was lower in dep2 mutant lines, suggesting feedback regulation of OsRING80 by DEP2. Remarkably, knocking out OsRING80 through CRISPR/Cas9-mediated gene editing resulted in greater resistance to M. oryzae without compromising plant growth. These findings reveal that OsRING80 plays a crucial role in balancing plant immunity and growth by targeting DEP2; they also provide a valuable candidate gene for developing improved rice cultivars with both disease resistance and optimal agronomic traits.

The ubiquitin-proteasome system (UPS) plays crucial roles in cellular processes including plant growth, development, and stress responses. In this study, we report that a pair of E3 ubiquitin ligases, AvrPiz-t-interaction protein 6 (APIP6) and IPA1-interaction protein 1 (IPI1), intricately target early flowering3 (ELF3) paralogous proteins to control rice immunity and flowering. APIP6 forms homo-oligomers or hetero-oligomers with IPI1. Both proteins interact with OsELF3-2, promoting its degradation to positively control resistance against the rice blast fungus (Magnaporthe oryzae). Intriguingly, overexpression of IPI1 in Nipponbare caused significantly late-flowering phenotypes similar to the oself3-1 mutant. Except for late flowering, oself3-1 enhances resistance against M. oryzae. IPI1 also interacts with and promotes the degradation of OsELF3-1, a paralog of OsELF3-2. Notably, IPI1 and APIP6 synergistically modulate OsELF3s degradation, finely tuning blast disease resistance by targeting OsELF3-2, while IPI1 controls both disease resistance and flowering by targeting OsELF3-1. This study unravels multiple functions for a pair of E3 ligases in rice.

Plants typically activate distinct defense pathways against various pathogens. Heightened resistance to one pathogen often coincides with increased susceptibility to another pathogen. However, the underlying molecular basis of this antagonistic response remains unclear. Here, we demonstrate that mutants defective in the transcription factor ETHYLENE-INSENSITIVE 3-LIKE 2 (OsEIL2) exhibited enhanced resistance to the biotrophic bacterial pathogen Xanthomonas oryzae pv oryzae and to the hemibiotrophic fungal pathogen Magnaporthe oryzae, but enhanced susceptibility to the necrotrophic fungal pathogen Rhizoctonia solani. Furthermore, necrotroph-induced OsEIL2 binds to the promoter of OsWRKY67 with high affinity, leading to the upregulation of salicylic acid (SA)/jasmonic acid (JA) pathway genes and increased SA/JA levels, ultimately resulting in enhanced resistance. However, biotroph- and hemibiotroph-induced OsEIL2 targets OsERF083, resulting in the inhibition of SA/JA pathway genes and decreased SA/JA levels, ultimately leading to reduced resistance. Our findings unveil a previously uncharacterized defense mechanism wherein two distinct transcriptional regulatory modules differentially mediate immunity against pathogens with different lifestyles through the transcriptional reprogramming of phytohormone pathway genes.