Calcium (Ca2+) is an essential macronutrient for plant growth and defence, yet the molecular mechanisms regulating its uptake from soil remain largely undefined. Through bioinformatics and electrophysiological screening, we identified a group of plant-specific proteins, named the IONIC CURRENT FAMILY A (ICAs), which confer Ca2+-permeable non-selective cation channel (CNCC) activities in heterologous systems. In Arabidopsis thaliana, AtICA1, AtICA2, AtICA3 and AtICA4 are predominantly expressed in root cells, and their proteins localize to the plasma membrane. Under either limited or excessive external Ca2+ conditions, ica1/2/3/4 quadruple mutants display hypersensitivity or reduced sensitivity, respectively, as evidenced by altered root length. In addition, these mutants show increased sensitivity to various abiotic and biotic stresses under normal Ca2+ conditions. The ica mutants lack the previously characterized CNCC-mediated currents in roots that facilitate cellular Ca2+ uptake, resulting in lower Ca2+ levels compared with wild-type (WT) plants. Our findings suggest that AtICA1/2/3/4 may function as components of CNCCs, mediating Ca2+ uptake crucial for broad environmental stress tolerance under normal Ca2+ conditions. This study provides molecular insight into the mechanisms governing Ca2+ uptake in plant roots and expands our understanding of how plants maintain Ca2+ homeostasis under varying environmental conditions.

Abstract Recombination in polyploid genomes is generally constrained to homologous or homoeologous chromosomes; however, how chromosomal rearrangements influence recombination between chromosomes remains unclear. Here, we demonstrate that large-scale chromosomal rearrangements in the wild relatives of wheat are associated with recombination involving non-homoeologous chromosomes or arms during alien gene introgression under conditions that permit homoeologous recombination mediated by ph1b . Using a wheat chromosome 6A monosomic-induced 6AS•6CL Robertsonian translocation combined with ph1b -mediated recombination, we generated 17 independent recombinants carrying a new stem rust resistance gene, Sr69 , from Aegilops caudata chromosome arm 6CL. Unexpectedly, 94.1% (16 of 17) of recombinants resulted from exchanges with wheat group-7 chromosomes rather than with the homoeologous group-6 chromosome. Comparative sequence- and marker-based analyses identified a 67-Mb rearranged interval on Ae. caudata 6CL that corresponds to telomeric regions of the long arms of wheat group-7 chromosomes. Sequence similarity within this interval was quantitatively associated with recombination frequency, with higher similarity corresponding to more frequent translocations. Physical and optical mapping showed that recombination within the rearranged interval generated compensating 7A/6C, 7B/6C, and 7D/6C translocations, whereas recombination outside this region produced non-compensating 6A/6C exchanges. An independent case involving the powdery mildew resistance gene Pm7C showed a similar correspondence between a rearranged 7CL region and preferential introgression into wheat 7DS. Together, these results indicate that ph1b -mediated recombination involving structurally altered chromosomes is driven by local chromosomal structure and sequence similarity rather than strict homoeologous group identity. This provides a mechanistic basis for harnessing untapped beneficial genes from structurally rearranged alien genomes. Significance Statement Alien gene introgression is a powerful strategy for wheat improvement, typically relying on ph1b -mediated recombination between homoeologous chromosomes. The genomic basis and outcomes of introgression from structurally rearranged alien chromosomes remain unclear. Here, we show that ph1b -induced recombination can efficiently target wheat-allosyntenic blocks in rearranged alien genomes, preferentially transferring genes from structurally altered alien segments into their syntenic regions on wheat chromosomes of different homoeologous groups. Crossover formation is governed by extended sequence similarity within corresponding intervals rather than strict collinearity across entire homoeologous chromosomes. As many wild species exhibit extensive genome rearrangement, these findings and methodologies expand access to underexploited genetic diversity embedded within highly rearranged wild genomes for wheat improvement.

Shoot branching exhibits significant plasticity and is largely regulated by BRANCHED1 (BRC1), a key integrator of endogenous and environmental cues that acts locally to control axillary bud development. However, the gene regulatory networks governed by BRC1 and the mechanisms underlying its regulation remain poorly understood. Here, we identify a cluster of transcription factor-encoding genes that are dynamically responsive to multiple branching pathways, inversely correlated in expression with BRC1 levels, and functionally enriched in pathways related to floral organ development (FOD) and shoot system morphogenesis. Mechanistically, the heterotrimeric Nuclear Factor Y (NF-Y) complex is required for transcriptional activation of representative FOD genes, functioning through chromatin looping and H3K27me3 demethylation to establish active chromatin states at target loci. In contrast, BRC1 inhibits NF-Y complex assembly and its epigenetic regulatory effects in a dose-dependent manner, thereby enabling tunable FOD gene expression and plastic bud development. These findings position BRC1 as a molecular rheostat of NF-Y-dependent epigenetic regulation, providing mechanistic insights into the dynamic control of axillary bud development. Shoot branching plasticity is largely regulated by BRC1. The authors show that BRC1 acts as a dose-dependent rheostat, modulating NF-Y-mediated chromatin looping and H3K27me3 demethylation at floral organ development genes to fine-tune axillary bud activity.

Drought recovery and submergence confer hypoosmotic stress that disrupts plant cellular homeostasis and compromises growth and survival. Although calcium signaling serves as a central hub for plant adaptation to osmotic perturbations, the molecular mechanisms underlying hypoosmotic responses remain poorly understood. In this study, we identified COSR1 (Calcium-permeable Osmotic Stress Response 1) and its homolog COSR2 as Ca2+-permeable channels that are activated by hypoosmotic stimuli. Genetic analyses revealed that COSR1 plays a predominant role, with COSR2 serving a secondary compensatory role, as the cosr1 cosr2 double mutant exhibited substantially more severe phenotypes than either single mutant under post-drought recovery and submergence. Calcium imaging further demonstrated that COSR1 and COSR2 collectively mediate the second spike of hypoosmotic-induced Ca2+ influx, which is closely associated with TCH2/TCH4 induction and stress tolerance. Together, our work establishes that COSR1 and COSR2 are key components of the hypoosmotic-responsive signaling machinery that translates post-drought recovery and submergence-induced osmotic stress into Ca2+ signals, providing novel targets for improving crop resilience.

Widespread potassium (K) deficiency in paddy soils, coupled with the low potassium use efficiency (KUE) of rice, has driven research on genetically improving KUE for sustainable rice production. Breeding high-KUE rice cultivars requires thorough understanding of root K+ uptake molecular mechanisms mediated by specific K+ channels and transporters. Here, we characterize the Shaker-type K+ channel OsKAT1 in rice. Disruption of OsKAT1 impairs root K+ uptake, resulting in reduced K+ accumulation and severe growth retardation under low-K+ stress. Conversely, overexpression of OsKAT1 enhances root K+ acquisition and promotes rice growth. Notably, OsKAT1-overexpressing lines exhibit increased culm diameter and improved bending resistance, thereby enhancing lodging tolerance. OsKAT1 overexpression also significantly increases grain size and weight under both K+-sufficient and low-K+ conditions. Natural variation at the OsKAT1 locus correlates with differential gene expression among haplotypes, with Hap 2 and Hap 3 conferring superior tolerance to low-K+ stress. Additionally, our results suggest that the expression pattern and physiological function of OsKAT1 may be cultivar-dependent. Collectively, these findings establish OsKAT1 as a key integrator of low-K+ adaptation, lodging resistance, and yield enhancement in rice, offering a promising genetic target for breeding rice varieties with improved KUE and yield potential.

As sessile organisms, plants must continuously balance growth and stress adaptation in response to fluctuating environments. This balance is largely governed by two evolutionarily conserved kinase systems, the Target of Rapamycin Complex (TORC) and Snf1-Related Kinases (SnRKs). Under favorable conditions, plants adopt a “growth mode” in which sufficient nutrients, energy, and growth-promoting hormones activate TORC to drive anabolic metabolism, cell proliferation, and biomass accumulation. By contrast, under adverse conditions such as energy limitation, nutrient deprivation, and other environmental stresses, plants shift to an “adaptation mode” in which stress-associated cues, including low ATP, stress hormones (e.g., ABA), and Ca2+ transients activate distinct SnRK modules (SnRK1, SnRK2, and SnRK3/CIPKs) to promote catabolic reprogramming and enhance stress tolerance. Recent advances support a unifying model in which TORC and SnRKs reciprocally regulate each other, enabling plants to switch between growth and adaptation. In this review, we summarize how diverse growth-associated signals converge on TORC and how stress-specific signaling inputs selectively activate SnRK modules, and we highlight recent progress in elucidating the molecular mechanisms underlying TORC-SnRK crosstalk. We propose that the TORC-SnRK axis serves as a central signaling module that integrates energy, hormonal, and Ca2+ signals to coordinate growth and stress responses. This conceptual framework facilitates a mechanistic understanding on how plants optimize fitness in fluctuating environments and offers potential strategies for improving crop performance through targeted manipulation of this regulatory network.

Soil salinization poses a serious threat to plant development and represents a major obstacle to the sustainable production of crops worldwide. Melatonin (MT) contributes prominently to plant tolerance against abiotic environments. However, the molecular basis of transcriptional regulation underlying melatonin accumulation in tomato under saline-alkali stress is still largely unknown. Herein, we identify SlNAC2, a NAC transcription factor in tomato induced by saline-alkali stress, which suppresses the key melatonin biosynthetic genes SlCOMT2 and SlSNAT, while activating SlCV, a gene linked to reactive oxygen species (ROS) accumulation and programmed cell death. These regulatory effects reduce MT levels and promote excessive ROS production, ultimately altering the plant's tolerance to saline-alkali stress. Silencing of SlNAC2 through the RNA interference method significantly improves saline-alkali tolerance in tomato, while its constitutive overexpression shows increased susceptibility to saline-alkali stress. Further evidence reveals that under saline-alkali conditions, SlNAC2 directly targets cis-elements of SlCOMT2 and SlSNAT promoters, suppressing their transcription and consequently reducing melatonin levels, whereas simultaneously binding to the SlCV promoter to activate its expression, ultimately leading to ROS accumulation. Moreover, comprehensive protein interaction analyses confirmed that SlNAC2 physically associates with SlDREB2, a DREB-type transcription factor involved in salt stress response. Through its interaction with SlNAC2, SlDREB2 partially attenuates its repression of SlCOMT2 and SlSNAT, thereby increasing melatonin accumulation and ROS scavenging, ultimately enhancing tomato's resilience to saline-alkali stress conditions. Collectively, our findings reveal a SlNAC2-SlDREB2 regulatory module that finely tunes melatonin synthesis and ROS levels to regulate tomato's response to saline-alkali stress, providing new strategies for developing stress-resilient tomato varieties.

Rooted in place, plants must continuously respond and adapt to their ever-changing environment to survive, especially as climate change intensifies. Calcium ions (Ca²⁺) play a central role in plant responses to both biotic and abiotic challenges. Ca²⁺ signaling involves the coordinated action of channels and transporters that generate specific "Ca²⁺ codes," along with Ca²⁺-binding proteins that act as sensors to decode them. Studies over the past several decades have explored the molecular components that form the toolkit, pathways, and networks for the coding and decoding of Ca²⁺ signals in plants. This review focuses on the emerging mechanisms of calcium signaling in plants, beginning with an overview of the universal conceptual framework that governs the coding and decoding of Ca²⁺ signals, followed by examples of pathways in plant growth and reproduction, responses to abiotic stress and microbes, and systemic signaling in plants.

As the last stage of leaf development, senescence is orchestrated by an intricate network of endogenous factors and external signals to ensure an efficient recycling of nutrients. Hydrogen sulfide (H2S) serves as an important gaseous signaling molecule in plants, mediating a myriad of physiological processes like leaf senescence. However, the molecular mechanisms underlying H2S accumulation and its regulation during leaf senescence in tobacco are still not fully elucidated. In this work, we demonstrate that NtWRKY75, a WRKY transcription factor in tobacco (Nicotiana tabacum), serves as a negative regulator of the expression of the key genes involved in H2S biosynthesis (l-cysteine desulfhydrase, NtLCD1; d-cysteine desulfhydrase, NtDCD1), thereby accelerating dark-induced leaf senescence. The transcript levels of NtWRKY75 are progressively upregulated during both dark-induced and natural leaf senescence. Transgenic tobacco plants overexpressing NtWRKY75 show premature leaf senescence, while ntwrky75 mutants generated through CRISPR/Cas9 exhibit delayed leaf senescence. Further molecular and biochemical analyses reveal that senescence-associated NtWRKY75 binds to the promoters of NtDCD1 and NtOASA1, downregulating NtDCD1 expression while upregulating NtOASA1, thereby leading to decreased H2S accumulation. NtWRKY75 also interacts with the promoters of multiple amino acid transporter genes, including NtAAP3, resulting in their upregulation and facilitating amino acid remobilization, which accelerates leaf senescence. Additionally, NtVQ47, a protein containing the VQ motif, physically interacts with NtWRKY75 in vivo and in vitro, thereby fine-tuning its transcriptional activity and influencing leaf senescence. In conclusion, our findings demonstrate that the regulatory network composed of NtVQ47, NtWRKY75, and H2S plays a crucial role in precisely modulating leaf senescence, offering promising candidates and strategies for future crop improvement.

Adaptation to compound environmental stress is fundamental to plant survival.The phytohormone abscisic acid(ABA)serves as a central regulator of both biotic and abiotic stress responses(Lee and Luan,2012).Following environmental challenges,rapid ABA biosynthesis activates receptor-mediated signaling cascades,driving transcriptional reprogramming and post-translational mod-ifications for stress adaptation(Cutler et al.,2010).Consequently,ABA perception constitutes a critical regulatory step.Recently,a landmark study by Ma et al.(2025)demonstrated that NRT1.1B(NITRATE TRANSPORTER 1.1 B),beyond its canonical role as a ni-trate transceptor(transporter and receptor)(Tsay et al.,1993;Ho et al.,2009;Hu et al.,2015),also functions as an ABA receptor.This bifunctional protein thus forms a competitive signaling hub in which nitrate and ABA act as competing ligands.Binding of nitrate or ABA to NRT1.1 B triggers distinct downstream signaling outputs,enabling plants to dynamically prioritize nutrient acquisition or stress defense programs(Figure 1).

Extracellular adenosine triphosphate (eATP) functions as a damage-associated molecular pattern in plant immunity. P2K1, a purinergic receptor with a cytoplasmic serine/threonine kinase domain, initiates ATP-responsive signaling cascades characterized by a rapid spike in cytosolic Ca²⁺, which acts as a critical second messenger. In this study, we identified the cyclic nucleotide-gated channel complex CNGC2-CNGC4 as essential for eATP-induced calcium signaling and bacterial resistance in plants. A biochemical link between eATP perception and CNGC2-CNGC4 function was established by demonstrating the physical association between the channel complex and the eATP receptor P2K1 at the plasma membrane. Furthermore, we discovered that P2K1 phosphorylates the CNGC2 subunit of the CNGC2-CNGC4 channel in response to eATP, establishing a phosphorylation-dependent mechanism that connects eATP perception to calcium influx. Through AlphaFold-Multimer prediction, electrophysiological assay, and genetic analysis, we identified serine residues S705 and S718 in CNGC2 as the key phosphorylation sites mediating P2K1-dependent channel activation and eATP-triggered immunity. Notably, P2K1 selectively phosphorylates CNGC2, in contrast to BIK1 that phosphorylates CNGC4 during pathogen-associated molecular pattern-triggered immunity. Together, these findings indicate that the CNGC2-CNGC4 channel complex serves as a core component of calcium-dependent plant immunity, with distinct kinases phosphorylating different subunits in response to specific immune elicitors.

Uncovering the mechanisms underlying stress-resistant traits in xerophytes thriving in harsh environments can aid the genetic improvement of crops. The xerophyte Zygophyllum xanthoxylum features high Na+ accumulation in leaves, mediated by the vacuolar antiporter ZxNHX1. Co-expression of ZxNHX1 and vacuolar H+-PPase gene ZxVP1-1 has been demonstrated to enhance the stress resistance and biomass of alfalfa. However, it remains unknown if ZxNHX1 outperforms its homologues from the Na+-excluding and stress-sensitive glycophytes such as Arabidopsis in enhancing plant stress resistance and yield. Here, we found that expression of ZxNHX1 conferred superior growth under salt stress in alfalfa, compared to the Arabidopsis homologue AtNHX1. When expressed in yeast, ZxNHX1 displays stronger Na+/H+ but weaker K+/H+ exchange activity than AtNHX1. Under both K+ sufficient and deficient conditions, an Arabidopsis atnhx1-1 mutant expressing ZxNHX1 accumulated higher Na+ and lower K+ concentrations, with more Na+ being sequestered into vacuoles and a larger proportion of K+ retained in the cytosol. This optimized cellular ion distribution ensures energy-conserving osmotic adjustment, leading to stronger stress resistance and higher biomass than plants expressing AtNHX1. Moreover, ZxNHX1 governed the root uptake and root-to-leaf transport of Na+ at the whole-plant level, whereas AtNHX1 acted mainly in K+ transport processes. We also identified a polar residue Thr265 in a membrane-spanning region of ZxNHX1 that influences its Na+ and K+ selectivity. These findings reveal a new energy-conserving, Na+-based osmotic adjustment mechanism that can enhance crop stress resistance without sacrificing yield, providing an effective way for utilizing saline soils to expand crop production into marginal lands.

Soil salinisation poses a significant threat to alfalfa (Medicago sativa L.) growth and development, limiting its productivity and hindering its widespread cultivation. Hydrogen sulphide (H2S) serves as an important gaseous signalling molecule in plants, mediating a myriad of physiological processes like salt tolerance. However, the molecular mechanisms underlying H2S accumulation and its regulation under salinity stress in alfalfa are still not fully elucidated. In this study, we demonstrated that MsNAC2a, a NAC transcription factor, is a negative modulator of salt stress resistance in alfalfa. Constitutive overexpression of MsNAC2a downregulated the expression of H2S biosynthesis-related genes, such as L-CYSTEINE DESULFHYDRASE1 (MsLCD1), and upregulated the O-ACETYLSERINE(THIOL)LYASE ISOFORM A1 (MsOASA1) gene, a key gene involved in H2S metabolism, while also suppressing the expression of reactive oxygen species (ROS) scavenging genes like MsCOX11, leading to a reduction in hydrogen sulphide levels and an increase in ROS accumulation, ultimately impairing the plant's salt tolerance. Furthermore, the AP2/EREBP-type transcription factor MsEREBP1 physically interacts with MsNAC2a both in vivo and in vitro, influencing its transcriptional activity and modulating salt stress responses in alfalfa. Conversely, silencing MsNAC2a enhanced salt stress resistance without affecting plant growth or yield. Collectively, our study highlights that MsNAC2a precisely regulates the homeostasis of salt stress responses and provides new insights into the mechanisms by which the cooperative interaction between MsNAC2a and MsEREBP1 fine-tunes the homeostasis of endogenous H2S levels, thereby influencing alfalfa's salt tolerance and offering valuable strategies for improving crop resilience under saline stress.

Soil salinity negatively affects crop yields worldwide. The dynamic transition between growth and salt stress responses helps plants cope with changing soil salinity status. However, the molecular mechanisms controlling such dynamic transitions remain poorly understood. Here, our study identified the target of rapamycin complex (TORC) as a central player in growth recovery from salt stress. We observed a rapid decline in TORC activity in Arabidopsis thaliana plants upon exposure to salt stress. Further investigation uncovered an intricate interplay between TORC and a salt response signaling network comprising calcineurin B-like (CBL) proteins and CBL-interacting kinases (CIPKs). Under standard growth conditions, Regulatory-Associated Protein of TOR (RAPTOR) promotes CBL-CIPK complex dissociation, thereby inhibiting CIPK. CIPK suppression is lifted under salt stress, and the activated CBL-CIPK complex phosphorylates RAPTOR, which in turn suppresses TORC activity. Thus, the reciprocal regulation of the TORC and CBL-CIPK modules orchestrates plant responses and adaptation to soil salinity.

Root gravitropism relies on gravity perception by the root cap and requires tightly regulated phytohormone signaling. Here, we isolate a rice mutant that displays root coiling in hydroponics but normal gravitropic growth in soil. We identify COILING ROOT IN WATER 1 (CRW1) encoding an ETHYLENE-INSENSITIVE3 (EIN3)-BINDING F-BOX PROTEIN (OsEBF1) as the causative gene for the mutant phenotype. We show that the OsCRW1-EIN3 LIKE 1 and 2 (OsEIL1/2)-ETHYLENE RESPONSE FACTOR 82 (OsERF82) module controls the production of reactive oxygen species in the root tip, subsequently impacting root cap stability, polar localization of PIN-FORMED 2 (OsPIN2), symmetric distribution of auxin, and ultimately gravitropic growth of roots. The OsEIL1/2-OsERF82 ethylene signaling module is effectively impeded by applying gentle mechanical resistance to root tips, including growing in water-saturated paddy soil. We further show that mechanosensing-induced calcium signaling is required and sufficient for antagonizing the ethylene signaling pathway. This study has revealed previously unanticipated interplay among ethylene, auxin, and mechanosensing in the control of plant gravitropism.

Membrane transporters, including ion channels and carriers, maintain ionic and nutrient homeostasis vital for growth and stress resilience in plants. Their activity is finely regulated, enabling dynamic responses to internal and external signals. Transporters often exist in an ‘autoinhibited’ resting state that can be switched on by post-translational modifications in response to environmental cues. Specifically, protein phosphorylation functions as a molecular switch that relieves autoinhibition of channels and carriers to modulate their activities. We examine the phospho-regulation of exemplary transporters involved in nutrient allocation, stress resistance, and signal transduction, providing a perspective on how plants orchestrate membrane transport processes to sustain ion and nutrient balance and adapt to environmental challenges.

Calcium is a crucial macronutrient and functions as a wide-spread signal in eukaryotes,ranging from yeast,plants to animals.As crucial second messengers,calcium ions(Ca2+)play indispens-able roles in plant growth and development,response to external stressors,and signal transduction by modulating downstream cel-lular responses,including gene expression,metabolic activities,and transport functions[1,2].

Ongoing soil salinization severely hampers plant growth and the sustainability of global crops production. Hydrogen sulfide (H2S), acting as a critical gaseous signaling molecule, plays a vital role in plant response to various environmental cues such as salt stress. Nonetheless, it is not well understood how the transcriptional network regulates H2S production in response to salt stress in tomato. Herein, we determine that the bHLH transcription factor SlbHLH92 functions as a transcriptional activator in tomato (Solanum lycopersicum L.), upregulating the expression of the L-CYSTEINE DESULFHYDRASE 1 (SlLCD1) gene involved in H2S biosynthesis, thereby enhancing the plants' tolerance to salt stress. When exposed to salt stress, overexpression of SlbHLH92 in tomato leads to enhanced salt tolerance compared to wild-type plants. In contrast, suppression of SlbHLH92 expression with RNAi silencing results in increased sensitivity to salt stress. Subsequent molecular and biochemical investigations confirm that the salt-induced SlbHLH92 upregulates the expression of SlLCD1, leading to an increase in H₂S levels, as well as other salt-responsive genes (SlCBL10 and SlVQ16), by directly binding to specific cis-elements in their promoter regions. Furthermore, the VQ-motif containing protein SlVQ16 physically interacts with SlbHLH92, thereby promoting an increase in its transcriptional activity. Taken together, our study reveals an emerging mechanism in which the SlbHLH92-SlVQ16-H2S signaling cascade contributes to enhancing salt tolerance in tomato, presenting potential genetic targets for breeding salt-tolerant tomato cultivars.

Plant roots exhibit localized immunity (LI) mainly in the transition zone (TZ) and elongation zone (EZ). Plasma membrane-localized receptor-like kinases (RLKs) can mediate the plant's response to rhizosphere bacteria. However, how RLKs are involved in triggering LI in roots remains unclear. Here we identified dual actions for the RLK FERONIA (FER) in the LI response of Arabidopsis (Arabidopsis thaliana). The FER cytoplasmic domain is cleaved and translocated to the nucleus (FERN) to activate LI in the TZ and EZ in response to colonization by beneficial and pathogenic bacteria. In the absence or cessation of bacterial infection, full-length FER is plasma membrane-localized to maintain growth. Upon colonization and invasion by a high titre of bacteria, mature RAPID ALKALINIZATION FACTOR23 peptide accumulates and activates the matrix metalloproteinase At2-MMP, which triggers FER cytoplasmic domain cleavage specifically in the TZ and EZ to activate LI. This work demonstrates that two molecular forms of a single RLK balance growth and immunity via LI activation in Arabidopsis roots.

Over-application of potassium (K) fertilizer in fields has a negative impact on the environment. Developing rice varieties with high KUE will reduce fertilizer for sustainable agriculture. However, the genetic basis of KUE in a more diverse and inclusive population remains largely unexplored. Here, we show that the transcription factor OsNAC25 enhances K+ uptake and confers high KUE under low K+ supply. Disruption of OsNAC25 by CRISPR/Cas9-mediated mutagenesis led to a considerable loss of K+ uptake capacity in rice roots, coupled with reduced K+ accumulation in rice and severe plant growth defects under low- K+ conditions. However, the overexpression of OsNAC25 enhanced K+ accumulation by regulating proper K+ uptake capacity in rice roots. Further analysis displayed that OsNAC25 can bind to the promoter of OsSLAH3 to repress its transcription in response to low- K+ stress. Nucleotide diversity analyses suggested that OsNAC25 may be selected during japonica populations' adaptation of low K+ tolerance. Natural variation of OsNAC25 might cause differential expression in different haplotype varieties, thus conferring low K+ tolerance in the Hap 1 and Hap 4 -carrying varieties, and the japonica allele OsNAC25 could enhance low K+ tolerance in indica variety, conferring great potential to improve indica low K+ tolerance and grain development. Taken together, we have identified a new NAC regulator involved in rice low K+ tolerance and grain development, and provide a potential target gene for improving low K+ tolerance and grain development in rice.