生命科学最新文献

MicroRNAs (miRNAs) are key regulators of plant development and stress adaptation. While conserved miRNAs have been extensively characterized, the agronomic roles of lineage-specific miRNAs in crops remain largely unexplored. Here, we demonstrate that tae-miR5048, a wheat-specific miRNA, functions as a master regulator concurrently modulating plant architecture and drought tolerance. Overexpression of tae-miR5048 enhanced early root growth, accelerated reproductive transition, and optimized plant architecture and grain morphology without compromising grain yield. Conversely, CRISPR/Cas9-mediated knockout of TaMIR5048 homoeologs impaired root development and delayed flowering, yet promoted vegetative growth and grain yield potential, revealing a bidirectional regulatory role. Cytological analysis showed that tae-miR5048 optimizes plant height, flag leaf size and grain dimension by fine-tuning cell proliferation and expansion in a tissue-specific manner. Moreover, tae-miR5048 confers drought resilience throughout the growth cycle by elevating osmolyte accumulation to maintain tissue water status and alleviating oxidative damage through suppression of ROS production and membrane lipid peroxidation. Mechanistically, degradome sequencing, RLM‑5' RACE, and transient co‑expression assays demonstrated that tae-miR5048 directly targets and downregulates multiple kinase genes, including receptor-like protein kinases and mitogen-activated protein kinases, thereby modulating key signalling hubs post-transcriptionally. Transcriptome profiling further revealed that tae-miR5048 fine-tunes architectural traits by regulating cellular growth-related genes and enhances drought tolerance through activation of stress-responsive and proline biosynthesis pathways. Collectively, our findings establish tae-miR5048 as a central integrator that balances plant architecture and drought adaptation, providing the first functional evidence for a lineage-specific miRNA as a promising target for breeding climate-resilient wheat varieties.

Salt-induced inhibition of tillering constrains rice plant architecture and yield potential. To clarify the molecular links between salt tolerance and tiller development, we compared physiological responses and tiller-bud transcriptomes of the salt-tolerant japonica cultivar Nipponbare (NIP) and the salt-susceptible cultivar Kongyu 131 (KY131) under salt stress. Time-resolved RNA sequencing revealed cultivar-specific transcriptional dynamics, suggesting that rapid acclimation and transcriptome stabilisation in tiller buds contribute to salt tolerance. Functional enrichment highlighted redox regulation, phenylpropanoid metabolism, chlorophyll biosynthesis, nitrogen metabolism, and phytohormone signalling as key processes coordinating salt adaptation and tiller-bud development. Co-expression analysis identified the NAC transcription factor OsNAC4 as a central regulatory hub. Functional analyses showed that OsNAC4 negatively regulates rice salt tolerance and tillering. Loss-of-function Osnac4 mutants exhibited enhanced salt tolerance, reduced ROS accumulation and membrane damage, increased antioxidant enzyme activities, and higher tiller number. Further analysis indicated that OsNAC4 functions as a transcriptional activator of stress-, redox-, metabolic-, and ABA-associated pathways, with OsNCED5 implicated as a downstream target mediating salt-induced ABA accumulation. Through integrated transcriptomic, physiological, and genetic evidence from comparative analyses, this study establishes a molecular connection between salt adaptation and rice tiller development and identifies candidate targets for breeding salt-tolerant rice with improved architecture.

Plants frequently encounter recurring, sequential and combined environmental stresses, yet their adaptive capacity cannot be explained solely by immediate signalling and short-term acclimation. Increasing evidence indicates that prior stress exposure can leave molecular, metabolic and physiological imprints that alter the magnitude, speed and quality of later responses, thereby giving rise to stress memory and adaptive plasticity. In plants, these persistent states are increasingly linked to epigenetic regulation, including changes in chromatin accessibility, histone modifications, DNA methylation, RNA-directed DNA methylation and non-coding RNA-mediated control. However, stress memory is not determined by chromatin regulation alone. It is also shaped by metabolic and cellular reprogramming involving osmolyte accumulation, redox buffering, energy redistribution, protein quality control, autophagy, selective protein turnover and membrane remodelling, all of which help sustain cellular homeostasis during stress and recovery. In parallel, chloroplasts, mitochondria and the endoplasmic reticulum act as stress-sensitive organelles that relay their functional state to the nucleus through retrograde signalling, while long-distance systemic communication mediated by reactive oxygen species, calcium waves, electrical and hydraulic signals, hormones and peptides coordinates whole-plant acclimation. This review synthesizes these layers into a unified framework and argues that plant resilience under fluctuating environments depends on the interaction between stress memory, metabolic plasticity, organelle-derived signalling and systemic acquired acclimation. Particular attention is given to the distinction between transient acclimation and true memory, the balance between maintenance and resetting of stress-induced states and the developmental and fitness trade-offs associated with persistent preparedness. This review also highlights major gaps that continue to limit the field, including the lack of standardized criteria for defining stress memory, insufficient causal validation of epigenetic marks, weak integration of chromatin and metabolic states with whole-plant phenotypes, and the limited translation of memory-associated mechanisms into crop performance under realistic field conditions. Overall, this review provides a comprehensive framework for understanding how plants not only respond to stress, but also encode, retain and deploy information from prior exposure to optimize subsequent adaptation.

The dehydration tolerance of photosynthetic tissues varies greatly along land plant's phylogeny. We investigated the photochemical response to severe dehydration and subsequent rehydration in 318 species representing the major terrestrial biomes and photosynthetic lineages: lichens, bryophytes, pteridophytes and spermatophytes. Using a standardized portable dehydration test with the maximum photochemical efficiency of PSII (F_v/F_m) as indicator, data meeting two key criteria were analyzed: (1) optimal physiological conditions before dehydration and (2) achieving relative water contents (RWC) below 25% at the dehydration stage (with approximately half dropping further to 5%-15%). Lichens and mosses displayed the highest overall Fv/Fm recovery after dehydration, whereas lower tolerance was observed in the other plant groups. Four distinct photochemical responses to dehydration emerged: dehydration-sensitive (61.2%), rehydration-sensitive (18.6%), dehydration-tolerant (13.6%), and dehydration-resistant (6.5%). Pteridophytes and spermatophytes predominantly exhibited dehydration- or rehydration-sensitive responses, whereas dehydration-tolerant dynamics were mainly observed in mosses and resurrection plants. Dehydration-resistant patterns were rare and occurred particularly in polar and high-altitude angiosperms such as Colobanthus quitensis, Deschampsia antarctica and Pozoa coriacea. These findings highlight the evolutionary divergence of dehydration tolerance strategies across the land plant phylogeny and provide insights into the underlying photochemical mechanisms.

In plants, an adequate supply of Nicotinamide adenine dinucleotide phosphate (NADPH) in the cytosol is crucial for maintaining a variety of biosynthetic and antioxidant reactions. Cytosolic NADPH is mainly generated via four enzymatic pathways: NADP-dependent malic dehydrogenase (NADP-ME), cytosolic oxidative pentose phosphate pathway (cOPPP), cytosolic NADP-dependent isocitrate dehydrogenase (cyNADP-ICDH), and non-phosphorylating glyceraldehyde-3-phosphate dehydrogenase (np-GAPDH). Here, we employed the cytosolic NADPH sensor mCherry-iNAP1 along with a GUS reporter system and enzyme assays to clarify the contributions of the four NADP(H)-reducing pathways in Arabidopsis seedlings and mature leaves. Our results show that, in 5-day-old seedlings, cyNADP-ICDH and np-GAPDH supply cytosolic NADPH to both roots and shoots, cOPPP could contribute more cytosolic NADPH to roots than to shoots, and NADP-ME2 primarily functions in roots. In leaves of 21-day-old plants, cyNADP-ICDH and np-GAPDH supply cytosolic NADPH throughout the day, while cOPPP could be more active at night, and NADP-ME2 utilizes daytime-accumulated malate to produce substantial cytosolic NADPH at night. Spatiotemporal visualization of cytosolic NADPH through in vivo imaging provides crucial information for future redox engineering of stress-resistant crops.

Tropospheric ozone (O₃) reduces crop productivity, but the sites at which ozone alters photosynthetic electron transport remain unclear. We tested whether acute exposure to O₃ shifts the dominant site of electron transport limitation in a cultivar-specific manner, rather than causing a uniform decline in PSII function. The induction kinetics of chlorophyll a fluorescence in two wheat cultivars, PAN 3434 and PAN 3161, were analysed after controlled exposure to 100 ppb O₃ as an acute mechanistic perturbation, using charcoal-filtered air as a low-ozone reference treatment. O₃ induced different cultivar-dependent changes in fluorescence rise phases. In PAN 3434, suppression of the J-I and I-P phases were consistent with a restricted reduction of the plastoquinone pool and a reduced acceptor-side capacity of PSI, accompanied by declines in the density of the active PSII reaction centre and the probabilities of electron transport. In contrast, PAN 3161 showed smaller changes in these parameters, consistent with partial preservation of reaction centre function and intersystem electron transport. These contrasting photochemical signatures were associated with cultivar-specific yield reductions. The findings indicate that acute O₃ exposure alters distinct segments of the PSII-PSI electron transport chain in a cultivar-specific manner, providing mechanistic information relevant to physiological phenotyping and cultivar screening for ozone tolerance in wheat.

Soil salinisation severely constrains crop production. Legumes rely on rhizobial symbiosis for sustainable nitrogen acquisition. Although salinity is known to impair nodulation and nitrogen fixation, how symbiosis influences plant tolerance to salt stress remains unclear. In this study, we integrate physiological, biochemical, transcriptomic, ionomic, and metabolomic analyses to investigate the role of rhizobial symbiosis in salinity tolerance in Vicia sativa (common vetch) and Pisum sativum (pea). In both species, nodulated plants exhibited markedly enhanced survival and grain production under prolonged salt stress compared with nitrogen-fertilised (N-fed) controls. Under moderate salinity, nodulation helped maintain water status and stomatal conductance, reduced Na⁺ accumulation while improving K⁺ retention, and attenuated osmotic and oxidative stress, as evidenced by lower proline and malondialdehyde levels. Transcriptomic profiles in vetch revealed that symbiosis is associated with changes in the plant responses toward growth and microbial signalling, reducing the strong activation of stress pathways that typically occurs in non-nodulated plants. Ionomic and metabolomic data further showed that nodulated plants preserve nutrient balance and maintain a more stable carbon-nitrogen metabolism under salinity. These findings highlight the potential of Rhizobium inoculation to enhance crop resilience in salt-affected agroecosystems and demonstrate that symbiosis correlates with a more efficient and physiologically moderated acclimation to salinity in legumes.

Excessive nitrogen (N) application can affect soil health and crop performance, yet the multi-generational effects of prolonged high-N exposure on wheat seed germination remain unclear. We profiled seed metabolomes and endophytic bacterial communities across seven consecutive wheat generations (F1-F7) under normal-N and high-N regimes, and assessed germination of F7 seeds. Spatial metabolomics, spatial transcriptomics and 16S rRNA sequencing were used to resolve embryo- and endosperm-specific responses. Seven generations of high-N treatment delayed progeny seed germination and decreased the germination index by 12.3%, whereas the vigor index was not significantly affected. Spatial omics revealed strong embryo-endosperm heterogeneity and a high-N-associated shift in endosperm metabolism, including a 73.9% decrease in endosperm L-aspartic acid. Compartment-resolved microbiome analysis showed enrichment of Bacillus under high-N exposure. Functional assays showed that L-aspartic acid promoted germination/early outgrowth, whereas Bacillus grew with L-aspartic acid as the sole C/N source and reduced germination under L-aspartic acid-supplemented conditions. These results support a model in which multi-generational high N reduces wheat seed germination through endosperm amino-acid depletion and altered endophytic bacterial assembly.

Botrytis cinerea is a devastating necrotrophic pathogen threatening global agriculture. Although modulating light intensity holds promise for sustainable disease management, the regulatory strategies and underlying mechanisms remain largely undefined. Three light intensity levels (200, 500 and 800 µmol·m^-2·s^-1) were applied in this study. By integrating multilevel pathological and cytological observations with transcriptional and metabolic pathway analyses, we systematically investigated how light intensity regulates defence responses against B. cinerea in tomato (Solanum lycopersicum). The results revealed that 200 µmol·m^-2·s^-1 light most effectively attenuated disease progression by orchestrating a multilayered defence network. This network encompasses stomatal closure to restrict pathogen invasion, phenylalanine-derived lignin biosynthesis for cell wall reinforcement, upregulation of pathogenesis-related proteins to facilitate pathogen degradation and maintenance of redox homeostasis to mitigate oxidative damage. These coordinated responses, rather than direct pathogen inhibition by light intensity, collectively restrict B. cinerea invasion. Application of exogenous phenylalanine and the PAL inhibitor 2-aminoindan-2-phosphonic acid (AIP) further validated that light intensity dictates metabolic flux partitioning within the phenylpropanoid pathway, a core mechanism for enhanced resistance. This study provides the first evidence that low-light-induced resistance to B. cinerea stems from phenylpropanoid metabolic reprogramming and ROS homeostasis, offering novel insights into light-modulated plant defence against necrotrophic pathogens.