The Plant Journal最新文献

Interactions between phosphate (Pi) and zinc (Zn) or iron (Fe) nutrition in plants have been widely studied; however, the underlying mechanisms of their cross-talks in arbuscular mycorrhizal (AM) plants remain obscure. Here, we examine the physiological and molecular responses of tomato (Solanum lycopersicum L.) to the combination of Pi, Zn and/or Fe nutrient stresses during symbiosis with Rhizophagus irregularis, revealing the existence of a tripartite Pi-Zn-Fe cross-talk in AM symbiosis. Interestingly, the mycorrhiza-activated SlPT3, a member of the PHOSPHATE TRANSPORTER 1 (PHT1) gene family in tomato, is remarkably induced upon the simultaneous Pi and Zn deficiencies. Reverse genetics analysis revealed that SlPT3 not only contributes to Pi transport but is also essential for arbuscule development during Zn deficiency. Moreover, knockdown of SlPT3 leads to reduced Fe accumulation and arbuscule degeneration in mycorrhizal roots by integration of Pi and Zn deficiencies. In silico analysis indicated that the SlPT3 and its homologs contain the IRT (Iron-regulated transporter) domain across dicot and monocot species. Further heterogeneous expression of SlPT3 in yeasts can restore the Δpho84 defects in high-affinity Pi uptake and regulate iron (Fe⁺²) homeostasis in the fet3fet4 mutant. Collectively, SlPT3 serves as a context-dependent transporter that reshapes nutrient transport priorities in response to combined stresses, revealing a sophisticated mechanism for maintaining symbiosis under fluctuating soil nutrient conditions. These findings provide new avenues for exploring how arbuscular mycorrhizas integrate multiple nutrient stress signals into intricate plant development.

Drought and pathogen infection severely affect plant growth and development. The plant hormones abscisic acid and salicylic acid promote drought and disease resistance, respectively. However, it is largely unknown how plants balance these two stress responses. The salicylic acid receptor NPR1 is required for pathogen resistance and the transcription factors ABF3/4 are required for drought resistance. Here, we show that NPR1 negatively regulates drought resistance by inhibiting ABF3/4 in Arabidopsis. The npr1 mutant is more resistant to drought stress than wild type. Transcriptome analysis reveals that the npr1 mutant shows enhanced expression of the drought-responsive genes, in which the ABF-binding motif is significantly enriched. Genetically, loss of ABF3/4 suppresses the enhanced drought resistance of npr1. Biochemically, NPR1 physically interacts with ABF3/4 and functions as the adaptor protein of the cullin3-based E3 ubiquitin ligase CRL3^NPR1 to mediate the polyubiquitination and degradation of ABF3/4. Therefore, our study suggests that NPR1 antagonistically regulates drought resistance and disease resistance.

The Asian citrus psyllid (Diaphorina citri, ACP) is the primary vector of citrus Huanglongbing (HLB), the most devastating disease affecting the citrus industry. The effective management of ACP is crucial for preventing the spread of HLB. An environmentally friendly approach to pest control is the genetic enhancement of plants for improved insect resistance. WRKY transcription factors are known to play vital roles in plant defense against herbivores; however, their specific function in citrus resistance to ACP remains unexplored. This study demonstrated that the ACP-induced expression of CsWRKY40 plays a positive role in enhancing citrus resistance to ACP infestation. This was confirmed through both stable overexpression and virus-induced gene silencing (VIGS) assays in lemon plants (Citrus limon). Metabolomic analysis revealed that the overexpression of CsWRKY40 substantially affected flavonoids, particularly flavonol glycosides. Notably, the quercetin-3-O-glucoside content in CsWRKY40-overexpressing plants was significantly higher than in wild-type (WT) plants after ACP infestation, as confirmed by LC–MS analysis. Furthermore, the study revealed that CsWRKY40 directly binds to and activates the CsUGT89B1 promoter, driving the accumulation of the defense-related metabolite quercetin-3-O-glucoside, thereby enhancing resistance to ACP. Finally, CsERF1B was identified as a direct upstream transcriptional activator of CsWRKY40, which contributed to citrus resistance to ACP by activating the CsWRKY40-mediated defense pathway. These findings provide novel insights into the molecular mechanisms underlying CsWRKY40-mediated citrus defense against ACP and offer potential genetic targets for improving strategies to manage ACP and HLB in citrus cultivation.

Delaying the application of plant growth retardants, such as ethephon, can increase kernel number in maize (Zea mays L.), primarily due to the enhanced assimilate allocation to the ear. However, the underlying physiological and molecular mechanisms remain unclear. To clarify this, we investigated the effects of ethephon application from the 8- to 15-leaf stages (E8–E15) on the physiological mechanisms of kernel development, including internode elongation, dry matter accumulation and partitioning, fertilization, and kernel set. RNA-seq analysis was further performed on E14-treated and control (water spraying) plants at the silking stage and 8 days after silking to elucidate the molecular mechanisms underlying the ethephon-mediated kernel number increase. Delaying ethephon application at E14–E15 significantly shortened internodes below (−26.3% to −23.5%), at (−33.9% to −41.2%), and above (−22.9% to −52.5%) the ear. Average whole-plant dry matter increased by 8.1% at E14–E15 compared with the control. While ear dry matter increased by 32.4% at E14, it remained unchanged at E15. Optimizing the timing of ethephon application at E14–E15 did not negatively affect spikelet number formation but allocated more assimilates to the ear by retarding stem growth, resulting in increased kernel number (+8.3%) and grain yield (+7.4%). In E14, elevated sucrose allocation to the ear at silking resulted in increased trehalose-6-phosphate (T6P) accumulation, which subsequently enhanced assimilate import and improved carbohydrate utilization after flowering. Consequently, ear sucrose levels at silking were significantly higher than those in the control, consistent with the enhanced sink capacity. This enhancement was related to the suppression of sucrose-non-fermenting1-related protein kinase (SnRK1) activity. In contrast, post-flowering sucrose content was lower in E14 due to the upregulation of T6P–SnRK1 interaction genes during the kernel differentiation stage, which promoted sucrose utilization. Taken together, delayed ethephon application increased maize kernel number by optimizing pre-flowering sucrose partitioning to the ear and promoting post-flowering sucrose utilization.

Carrot (Daucus carota L.) is an important root vegetable crop of the Daucus genus in the Apiaceae. As the main product organ of carrot, the taproot has high nutritional and economic value. Expansins, a class of proteins involved in plant cell wall relaxation and cell extension, are mainly found in growing tissues and organs. Expansins play an important role in plant root development. Here, the DcEXP22 gene with a length of 789 bp was cloned from the carrot cultivar ‘Kurodagosun’. Based on the stable genetic transformation system and CRISPR/Cas9 gene-editing technology, the DcEXP22 gene was overexpressed and knocked out in carrots. The results indicated that overexpression of the DcEXP22 gene increased carrot root fresh weight, root diameter, and root-shoot ratio, and enlarged the perimeter and area of taproot phloem cells. In contrast, knockout of the DcEXP22 gene inhibited the development of carrot taproots and the extension of phloem cells, suggesting that the DcEXP22 gene might promote the enlargement of carrot taproots by regulating the size of phloem cells. RNA-seq analysis identified several genes that were co-expressed with DcEXP22, including DcCYP734A1, DcERF1, DcMAP2K1, and DcSAD9. It was hypothesized that the DcEXP22 gene might influence the enlargement of carrot taproot by participating in the signal transduction of phytohormones such as brassinosteroids, cell wall synthesis and modification, and fatty acid metabolisms. These findings will advance our knowledge of the molecular mechanisms of carrot taproot enlargement.

Nitrogen (N) is an essential macronutrient for plant growth and development; however, its low utilization efficiency in crops limits the sustainability of modern agriculture, primarily due to unclear regulatory mechanisms underlying N uptake and utilization. Identifying novel regulators of nitrate (NO₃⁻) signaling is critical for improving N use efficiency (NUE) in crops. Here, we identified the WRKY family transcription factor WRKY20 as a key regulator of NO₃⁻ signaling and metabolism in Arabidopsis thaliana. The expression of NO₃⁻-responsive genes was significantly suppressed in wrky20 mutants after NO₃⁻ treatment, suggesting that WRKY20 plays a key role in regulating NO₃⁻ signaling. NO₃⁻ content was significantly lower in the wrky20 mutants as a result of impaired uptake and assimilation. Genetic and molecular evidence indicates that WRKY20 functions downstream of NLP7 in the NO₃⁻ signaling pathway. Further investigation revealed that WRKY20 interacts with the negative regulator NIGT1.4 and antagonistically regulates NRT2.1 expression. Overexpression of WRKY20 promotes plant growth and enhances both seed yield and NUE. Together, these findings highlight the essential role of WRKY20 in regulating NO₃⁻ signaling and metabolism, providing a promising molecular target for improving NUE in crops.

The endogenous hydrogen (H₂) synthesis pathway in higher plants has been a mystery for nearly a century. Here, we report that the tomato Nuclear Architecture Related 1 (NAR1) protein is an enzymatic source of plant-based H₂. Mutation experiments found that the H₂-producing hydrogenase activity is closely related to four H-cluster coordinating cysteine residues and is positively regulated in darkness. Contrary changes in H₂ production and lateral root (LR) branching were individually observed in SlNAR1 overexpression and mutant lines. The homozygous lethal effect of knocking out tomato NAR1 was also observed. Genetic and anatomic evidence confirmed that NAR1 control of endogenous H₂ is a signaling mechanism that manipulates the expression of polar auxin transporters. Auxin accumulation in LR primordium and oscillation zone and LR branching stimulation were subsequently observed. Pot-cultured transgenic tomato plants overexpressing SlNAR1 display a luxuriant root system. These findings identify a mechanism for genetic engineering to regulate root organogenesis through alteration of NAR1-dependent H₂.

As a critical phase transition in plant development, seed germination is sensitive to salt stress. Several phytohormones including abscisic acid (ABA) and gibberellin (GA) are involved in the suppression of seed germination by salt stress. Emerging evidence suggests that long noncoding RNAs (lncRNAs) play a regulatory role in the response of plants to varying abiotic stresses. Many salt stress-responsive lncRNAs have been identified in different plant species; however, the molecular mechanisms underlying the epigenetic regulation of plant response to salt stress by lncRNAs remain largely unexplored. Here, we identified a salt stress-induced MtCIR2, a lncRNA in legume species Medicago truncatula, and found that overexpression and mutation of MtCIR2 led to reduced and enhanced seed germination under salt stress, respectively. The MtCIR2-dependent seed germination under salt stress was accounted for by an increase in the endogenous concentration of ABA and a decrease in the endogenous GA concentration. We further discovered that MtCIR2 interacted with BMI1, a core component of Polycomb Repressive Complex 1, which in turn enhanced H2A ubiquitination at the loci encoding ABA catabolic enzyme gene CYP707A2 and GA biosynthesis gene GA20ox1/2. This epigenetic silencing by MtCIR2 led to an increase in endogenous ABA and a decrease in GA concentration of germinating seeds, thereby suppressing seed germination under salt stress. These findings elucidate a novel mechanism by which lncRNA epigenetically regulates plant response to abiotic stress via histone ubiquitination, and highlight an intricate interplay between the lncRNA and epigenetic machinery in response to salt stress during seed germination.