Plant, Cell & Environment最新文献

Phytophthora nicotianae is a plant-pathogenic oomycete, posing a serious threat to global agriculture due to its highly destructive infections and challenges in management. To explore a biologically based disease management strategy, we investigated Streptomyces ardesiacus HL-06, which produces phenazine-1-carboxamide (PCN), a potent anti-oomycete metabolite that effectively suppresses the growth of P. nicotianae in vitro and reduces tobacco black shank severity by over 80% under field conditions, surpassing the efficacy of commercial fungicides. Mechanistically, we identified CDC48, a AAA+ ATPase essential for mitochondrial homeostasis, as the direct molecular target of PCN. Drug affinity responsive target stability (DARTS), molecular docking, and isothermal titration calorimetry revealed that PCN binds to CDC48's ATPase domain, thereby disrupting mitochondrial protein quality control. This interaction leads to mitochondrial cristae loss, ATP synthase inhibition, and reactive oxygen species (ROS) accumulation, ultimately triggering oomycete apoptosis. This is the first report of a phenazine compound targeting a eukaryotic AAA+ ATPase, revealing a novel mode of action against oomycete pathogens. Our findings integrate microbial ecology with chemical biology, positioning PCN as a promising eco-friendly candidate for sustainable plant disease management.

Common mycorrhizal networks (CMN) formed by arbuscular mycorrhizal (AM) fungi are critical pathways for plant nutrition and interplant nutrient transfer. However, their role in mediating sexually asymmetric interactions in dioecious plants remains poorly understood, especially under nitrogen (N) deficiency. Using in vivo ¹⁵N leaf-labeling in Populus cathayana saplings, we quantified N transfer via CMN between sexes and linked them to root traits. We found that intersexual pairs facilitated CMN-mediated N transfer from male to female saplings; this transfer was markedly amplified under low N conditions. When N availability shifted from sufficient to deficient conditions, males shifted from a conservative strategy to an AM fungi-dependent 'outsourcing' strategy (characterized by higher mycorrhizal colonization rates), whereas females transitioned from a relatively weak root foraging strategy to an enhanced one (with greater specific root length and specific root area). This strategic divergence promoted sexually asymmetric N transfer via CMN, leading to optimized nutrient use efficiency at the population level. These results highlighted a previously unrecognized role of CMN in facilitating sexually asymmetric nutrient interactions, offering a mechanistic framework to improve both productivity and sustainability in dioecious plantations on nutrient-poor soils.

Wheat natural resistance-associated macrophage protein 3 (NRAMP3) are manganese (Mn) transporters that can also transport unwanted cadmium (Cd). However, their roles in regulating grain Cd concentration are unknown. Here, we functionally characterised TpNRAMP3-7A and TpNRAMP3-7B cloned from dwarf Polish wheat (Triticum polonicum L., AABB) in them of their expression patterns, transcript localisations, metal transport activities, and associated phenotypes. Both TpNRAMP3-7A and TpNRAMP3-7B were expressed in the epidermis, endodermis, and xylem parenchyma cells of roots, the xylem parenchyma cells and phloem region of nodes and leaf sheaths, and the phloem region of leaf blades. Knockout of TpNRAMP3-7A and/or TpNRAMP3-7B not only limited grain Cd concentration, but also reduced Cd uptake, root-to-shoot translocation, and shoot-to-grain distribution. They also limited grain Mn concentration by inhibiting shoot-to-grain Mn distribution when grown in the field (high-Mn concentration), and decreased Mn uptake and root-to-shoot translocation under low-Mn stress. Position 192F in TpNRAMP3 was the core amino acid determining Cd and Mn transport activity. These results provide a valuable guide and target gene for limiting Cd concentration in wheat grains.

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.

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.