Plant, Cell & Environment最新文献

Rice is a major crop in China with a strong tendency to accumulate cadmium (Cd), posing serious risks to grain safety. α-Ketoglutarate (AKG), a key tricarboxylic acid cycle intermediate, has known roles in abiotic stress responses, but its effects on Cd tolerance and accumulation in rice remain unexplored. Exogenous AKG (50 μmol/L) was applied to investigate the mechanism regulating Cd tolerance and accumulation under both hydroponic and soil conditions. Under hydroponic experiments, exogenous AKG significantly reduced Cd translocation by 56.8%-63.9%, and decreased shoot Cd accumulation by 54.9%-60.6%. It alleviated photoinhibition and oxidative damage by enhancing photosynthesis and antioxidant activities while lowering H₂O₂ and MDA. Mechanistically, multi-omics analyses showed AKG confers Cd tolerance and Cd restriction concentration dependently. Under moderate Cd stress, AKG predominantly enhances the ascorbate-glutathione cycle and flavonoid biosynthesis for antioxidative defence, while upregulating OsHMA3 and reinforcing the endodermal barrier to restrict Cd transport. Under severe Cd stress, AKG shifts to activating melatonin biosynthesis and further suppressing transporters like OsIRT1. Additionally, AKG reduced grain Cd by 40.7% and increased yield by 31.6% under soil conditions. These results demonstrated the effective role of AKG in integrated Cd mitigation and provide a novel strategy for safe rice production in Cd-contaminated soils.

Retrograde transport from endosomes to the trans-Golgi network (TGN) is essential for intracellular trafficking, yet its molecular mechanism remains poorly understood. In Fusarium graminearum, 10 Rab GTPases associated with the Golgi-associated retrograde protein (GARP) complex were identified through immunoprecipitation followed by mass spectrometry (IP-MS). Among these, only the deletion of FgRAB6 disrupted the proper localisation of the GARP complex to the TGN. FgRab6 directly interacts with the GARP subunit FgVps52 via a conserved Q73 residue, which is critical for fungal growth and pathogenicity. Notably, this Q73-dependent interaction is evolutionarily conserved across eukaryotic species. Upon GTP activation, FgRab6 recruits FgVps52 to the TGN, thereby facilitating the assembly of the GARP complex through the sequential recruitment of additional subunits, including FgVps51, FgVps53 and FgVps54. The fully assembled GARP complex subsequently recruits the retromer complex and ensures the precise localisation of the SNARE proteins FgSnc1, FgTlg1 and FgTlg2 at the endosomes and the TGN. Disruption of this pathway severely compromises fungal development and virulence. Collectively, these findings identify a FgRab6-GARP-retromer-coordinated vesicle trafficking pathway that mediates the retrograde transport of SNARE proteins, which is critical for the pathogenicity of F. graminearum. This work provides new mechanistic insights into vesicular transport and highlights potential targets for antifungal intervention.

Citrus Huanglongbing (HLB), caused by 'Candidatus Liberibacter asiaticus' (CaLas), is the most devastating disease affecting the global citrus industry. Here, we reported that the CaLas effector SDE70 promotes HLB pathogenicity by targeting the citrus ubiquitination pathway. Transgenic expression of SDE70 in Wanjincheng orange (Citrus sinensis Osbeck) accelerated early CaLas proliferation, aggravated HLB symptoms, and increased susceptibility to citrus canker induced by Xanthomonas citri subsp. citri (Xcc). These results demonstrate that SDE70 functions as a broad-spectrum suppressor of citrus immunity. Mechanistically, SDE70 physically interacts with CsRUB2, a citrus ubiquitin-related protein. Furthermore, CsRUB2 overexpression in Wanjincheng oranges reduced resistance to HLB but enhanced resistance to citrus canker. Both SDE70 and CsRUB2 elevated salicylic acid (SA) and hydrogen peroxide (H₂O₂) levels in transgenic plants while lowering methyl salicylate (MeSA) levels. CsRUB2 also decreased jasmonic acid (JA). In contrast to the suppressive effect of SDE70, CsRUB2 enhanced the transcription of citrus immunity genes. Transient expression assays further demonstrated that the SDE70-CsRUB2 interaction dysregulates citrus immunity by perturbing SA, MeSA, JA, and H₂O₂ signals. These findings provide a theoretical basis for understanding citrus-CaLas interactions and breeding citrus varieties with broad-spectrum resistance to both HLB and citrus canker.

Freeze-thaw injury is a major cause of winter mortality in woody plants; however, the molecular mechanisms linking freeze-thaw stress to DNA damage and repair remain poorly defined. Here, we investigated the physiological thresholds of freeze-thaw injury in poplar and identified key regulatory components that enhance cold tolerance through improved DNA damage repair. Field temperature monitoring and differential scanning calorimetry revealed an effective freeze-thaw threshold of approximately 12°C, beyond which cumulative intracellular damage occurs despite the absence of extreme low temperatures. Integrated lncRNA, miRNA and mRNA sequencing demonstrated coordinated regulation of a DNA replication gene, PySLD5, by two long non-coding RNAs (MSTRG.19225.8 and MSTRG.19233.11) and the microRNA ptc-miR6476a. Functional assays, including pull-down, dual-luciferase and structural modelling, validated direct interactions among these RNAs and PySLD5. Overexpression of PySLD5 conferred enhanced cold tolerance, reduced electrolyte leakage and lower DNA fragmentation after freeze-thaw stress, whereas knockout lines showed severe cold sensitivity, disease susceptibility and reduced survival. Comet assays confirmed that repeated freeze-thaw cycles caused cumulative DNA damage. Together, these findings support a DNA damage accumulation model in which coordinated RNA regulation of PySLD5 promotes DNA repair, stabilizes replication forks and enhances overwintering survival.

Nitrogen (N) deposition has driven a tendency towards graminoid monodominance in alpine grassland plant communities on the Qinghai-Tibetan Plateau (QTP), but the molecular mechanisms underlying these changes remain poorly understood. Here, we selected Leymus secalinus, the most dominant species in alpine grasslands of the QTP under N addition, to characterise its adaptation to N addition by measuring integrated morphological, physiological traits, transcriptomics, proteomics and metabolomics at different simulated levels of N addition of 0 (CK), 8 (N1), 40 (N3) and 72 (N5) kg N ha^{- 1} yr^{- 1}. The results demonstrated that N addition significantly promoted the dominant growth of L. secalinus, enhancing its biomass and importance value. Under N addition, the expression of genes and proteins encoding key components of the photosystem (such as photosystem I and II proteins, antennae proteins, cytochrome b6f complex proteins, ferredoxin proteins) in L. secalinus was significantly up-regulated, enhancing its ability to compete for light resources. However, the enhancement of photosynthesis did not lead to the accumulation of soluble sugars and starch in L. secalinus. Instead, more carbon (C) skeletons and photosynthesis products were allocated to synthesise amino acids and their derivatives through the accelerated cyclic process of C and N metabolism to support the rapid growth of L. secalinus. Additionally, N addition obviously increased the antioxidant defence capacity of L. secalinus under the QTP's harsh environmental. These pathways might collectively contribute to the dominance of L. secalinus in alpine grassland on the QTP under N deposition, providing new insights into the response of alpine grassland plants to N deposition.

Drought events are becoming increasingly frequent and intense, posing major challenges to crop productivity. Beyond direct water stress, drought can indirectly affect plants by enhancing herbivore performance. While arbuscular mycorrhizal fungi (AMF) have been proposed to alleviate drought stress and to enhance plant resistance to herbivory, their role in mediating plant responses to the two combined pressures remains poorly understood. Here, we examined the individual and interactive effects of drought, AMF colonisation, and herbivory by Spodoptera exigua on maize (Zea mays) performance by combining a semi-field experiment with growth chamber assays. Drought reduced maize biomass (by 21.5%) and chlorophyll content (by 8.2%), while AMF improved reproductive traits. In particular, AMF colonisation increased the number of ears (from 1.1 to 1.4) and ear length (from 22.5 to 24.3 cm). Interestingly, drought transiently decreased DIMBOA-Glc levels in maize leaves, an effect that was exacerbated under AMF colonisation. Consistently, drought increased leaf herbivore performance by 32%. However, AMF colonisation mitigated the drought-induced increase in herbivore performance, even though leaf damage levels remained similar, indicating a post-ingestive resistance effect. This study highlights the need to consider multi-stressor interactions to harness AMF benefits in agriculture under increasing drought pressure.

Salicylic acid (SA) and jasmonic acid (JA) play critical roles in regulating plant disease resistance. However, the underlying molecular mechanisms of their coordinated action against pathogens in woody plants, particularly in peach (Prunus persica), are unknown. In this study, we demonstrate that SA and JA positively regulate resistance to bacterial spot disease induced by Xanthomonas arboricola pv. pruni (Xap) in peach. Two defence-responsive genes, pathogenesis-related protein 2 (PpPR2) and PpPR5, were induced to express during this disease response. A key transcription factor, TGACG-BINDING FACTOR 1 (PpTGA1), functioned as a positive regulator of disease resistance by activating PpPR2 and PpPR5 transcription. Furthermore, nonexpressor of pathogenesis-related gene 1 (PpNPR1), a core component of the SA signalling response pathway, interacted with PpTGA1 to enhance transcriptional activation of PpTGA1 on downstream PR genes, thereby strengthening disease resistance. The JA signalling repressor, JASMONATE ZIM-DOMAIN 1 (PpJAZ1), negatively regulated disease resistance by interacting with PpTGA1 and inhibiting its transcriptional activation on the PRs. In summary, this study reveals an important regulatory network mediated by SA-JA hormone crosstalk for peach resistance to bacterial spot disease, based on the PpNPR1/PpJAZ1-PpTGA1-PpPR2/5 cascade. These findings provide novel insight into the synergistic crosstalk between hormones and the defence mechanisms against bacterial spot disease.