Rapeseed (Brassica napus) is one of the most important oilseed crops worldwide, with its seed oil content (SOC) and quality directly determining its economic value. To resolve the challenges of growing demand for vegetable oil and advancements in rapeseed production, substantial progress has been achieved in the genetic improvement of SOC. This review systemizes genetic optimization strategies across three hierarchical processes: source expansion via enhanced photosynthesis, optimized carbon allocation, and metabolic redirection of photoassimilates; sink enhancement through targeted elevation of fatty acid (FA) synthesis, triacylglycerol (TAG) assembly, and seed coat development coupled with suppression of lipolytic pathways; flow optimization by modifying carbon partitioning, sucrose phloem loading and channeling to developing seeds. We synthesize reported genetic determinants of these processes and underscore their potential for enhancing SOC. Furthermore, we postulate that synergistic integration of source–flow–sink coordination with push–pull–package–protect frameworks could maximize oil accumulation, thereby establishing a multi-tiered roadmap for transcending SOC ceilings in rapeseed.

Salt stress, especially the increasing secondary salt stress, severely compromises apple production worldwide. Mitigation of oxidative damage caused by salt stress is critical for salt tolerance in apple plants. However, it remains unclear how the salt signal triggers the excessive reactive oxygen species (ROS) mitigation system in apple. In this study, we identified a salt-induced gene MdGRF10 (encoding a 14-3-3 protein), whose overexpression conferred transgenic apple plants reduced oxidative damage and enhanced salt tolerance. Furthermore, a salt-activated receptor-like cytoplasmic kinase MdPBL34 was found to interact with and phosphorylate the C-terminal of MdGRF10. This phosphorylation promoted the interaction between MdGRF10 and a melatonin rate-limiting synthetase MdASMT1 (N-acetylserotonin methyltransferase). Its overexpression or knockdown by CRISPR/Cas9 in transgenic apple plants demonstrated that MdASMT1 is critical in melatonin-mediated ROS scavenging for salt tolerance. Their interaction stabilizes MdASMT1 by decreasing its ubiquitin-mediated degradation for increased melatonin level, decreased oxidative damage and therefore promoted salt tolerance. Our findings revealed that 14-3-3 protein could integrate the salt signal in a phosphorylation-dependent manner. Moreover, MdPBL34 was also identified for the first time to be involved in salt signaling. Our research uncovered a novel MdPBL34–MdGRF10–MdASMT1 regulatory module in response to salt stress in apple, which will contribute to the molecular breeding of melatonin-enriched salt-tolerant apple trees.

Hydrogen sulfide (H₂S), a well-established gaseous signaling molecule, can effectively enhance plant tolerance to various environmental stresses. However, there is still a lack of suitable methods to release H₂S in agricultural production, and the mechanism by which H₂S improves stress resistance remains poorly understood. Here, we show the novel role of sodium butyrate (NaB) in producing H₂S consistently in rice rhizosphere soil and the epigenetic mechanism of H₂S to enhance rice drought tolerance. We found that NaB increased sulfate-reducing bacteria (SRB) abundance in the rhizosphere soil, resulting in higher expression of sulfite reductase (SiR), and consequently increased H₂S production. Mechanistic investigation showed that H₂S enhanced the level of H4K5ac in promoter regions of drought-tolerant genes, facilitating their expression by repressing the histone deacetylase (HDAC) gene OsHDA710. Loss-of-function mutants of OsHDA710 exhibited enhanced drought tolerance compared to wild-type (WT) plants, while OsHDA710 overexpression plants showed drought hypersensitivity. Moreover, we demonstrated that OsHDA710 could bind directly to promoters of drought-tolerance genes by recognizing the TGACC motif. Our findings illustrate an efficient way to produce H₂S and a novel mechanism for H₂S in improving the drought resistance of plants.

Hyperosmolality-triggered physiological drought hinders plant growth and development, leading to a drop in crop yields. Hyperosmolality triggers calcium signaling, and yet how osmotic-induced calcium signaling participates in cellular osmotic response remains enigmatic. To date, several Ca²⁺ channels and transporters have been identified to regulate osmotic-induced calcium signal generation (CaSG) or Ca²⁺ homeostasis. However, there has been no report on their function in calcium signal clearance (CaSC) in plants, especially in crops. Here, we investigated the role of a rice cation/calcium exchanger OsCCX2 in modulating calcium signaling dynamics using two distinct calcium reporters aequorin and GCaMP6s. The results showed that, under osmotic stress conditions, CaSC was significantly delayed in both root and guard cells of ccx2 mutants compared with the wild-type. Further studies revealed that hyperosmotic stress-triggered influxes of sodium (Na⁺), potassium (K⁺), and chloride (Cl⁻) ions were significantly reduced in ccx2 mutants, resulting in a significantly smaller range of osmotic pressure and water potentials (Ψ_w) adjustment. In addition, the stomatal response was impaired, with a faster water loss in ccx2 in response to hyperosmotic stress. Furthermore, the absence of OsCCX2 altered the expression patterns of key osmotic-responsive genes, but their transcriptional activation was unaffected. Collectively, these changes ultimately led to reduced hyperosmotic stress tolerance in the mutants. Additionally, OsCCX2 is likely to be located in the endoplasmic reticulum and plasma membrane, and possess Na⁺/Ca²⁺ exchange activity. To sum up, our findings provide evidence that OsCCX2, as a CaSC regulator, is involved in cell osmotic adjustment, water homeostasis and osmotic stress tolerance in rice, which offers new insight into potential applications in drought-resistant crop improvement.

In higher plants, stomatal movements represent a critical physiological process that matains cellular water homestasis while enabling photosynthetic gas exchange. Open stomata 1 (OST1), a key protein kinase in the abscisic acid (ABA) signaling cascade, has been established as a central regulator of stomatal dynamics. This study reveals that two highly conserved mitogen-activated protein kinase 1 (MAP4K1) and MAP4K2 are positive regulators in ABA promoted stomatal closure, and ABA-activated OST1 potentiates MAP4K1/2 through phosphorylation at conserved serine and threonine residues (S166, T170, and S479/S488). The activated MAP4K1, in turn, phosphorylates two critical downstream targets: plasma membrane H⁺-ATPase 2 (AHA2) at residues T858, T881, and Y946, and slow anion channel-associated 1 (SLAC1) at T114 and S116. Functional analysis demonstrates that the phosphomimetic (3D: S166D/T170D/S479D) MAP4K1, but not non-phosphorylatable (3A: S166A/T170A/S479A) MAP4K1, could fully restore drought tolerance and reduced water loss in detached leaves of map4k1map4k2 double mutant. Our findings delineate a previously unrecognized signaling module comprising OST1–MAP4K1/2–AHA2/SLAC1, which crucially modulates ABA-mediated stomatal regulation. This work advances our mechanistic understanding of phosphorylation cascades governing plant water relations and stress responses.

Both biotic and abiotic factors are expected to drive species diversification, yet demonstrating their synergistic effects within a single framework is challenging and has rarely been studied. The recent and rapid radiation of the genus Aspidistra (cast-iron plant) provides an ideal system for examining these processes. Here, we generated restriction site-associated DNA sequencing data for 123 Aspidistra taxa and reconstructed well-resolved phylogenies using both concatenation- and coalescent-based approaches. Using a comprehensive suite of diversification models, we quantified the contributions of multiple biotic and abiotic factors and applied phylogenetic path analysis to detect their synergistic effects. Our phylogenetic analyses recovered two main clades that differ in stem habits. We found that the diversification of Aspidistra has been driven by both abiotic factors (paleotemperature and the East Asian monsoon) and biotic factors (interspecific competition and pollination mutualism). Notably, these drivers operated both independently and synergistically to facilitate the rapid radiation of Aspidistra. Beyond providing a robust phylogeny useful for classifying Aspidistra, we present a statistical framework for better understanding the macroevolutionary processes underlying rapid plant radiations. Our findings underscore the critical importance of integrating multiple biotic and abiotic drivers into a unified analytical framework to comprehensively understand diversification history.

Eukaryotic photosystem I (PSI) is a multi-subunit pigment–protein supercomplex that consists of a core complex and multiple peripheral light-harvesting complexes I (LHCIs), which increases the light absorption capacity of the core complex. Throughout the evolution of oxygenic photoautotrophs, the core subunits of PSI have remained highly conserved, while LHCIs exhibit significant variability, presumably to adapt to diverse environments. This study presents a 2.82 Å resolution structure of PSI from the filamentous yellow-green alga Tribonema minus (Tm), a member of the class Xanthophyceae that evolved from red algae through endosymbiosis and is considered a promising candidate for biofuel production due to its high biomass and lipid content. Our structure reveals a supramolecular organization consisting of 12 core subunits and 13 LHCIs, here referred to as Xanthophyceae light-harvesting complexes (XLHs), along with the arrangement of pigments within the TmPSI–XLH supercomplex. A structural comparison between TmPSI-XLH and PSI–LHCI from various red lineages highlights distinctive features of TmPSI–XLH, suggesting that it represents a unique intermediate state in the PSI assembly process during the evolutionary transition from red algae to diatoms. Our findings advance the understanding of the molecular mechanisms responsible for energy transfer in Xanthophyceae PSI–XLH and the evolutionary adaptation of red lineages.

The anthracnose caused by Colletotrichum gloeosporioides poses a significant threat to the global mango (Mangifera indica L.) fruit industry. Although histone deacetylases (HDACs) are well recognized to be involved in plant immunity, the role of HDAC-mediated nonhistone deacetylation in the fruit immune response remains elusive. In the present study, MiHDA3, an HDAC from the RPD3/HDA1 subfamily, was identified as a candidate for regulating mango resistance based on the greatest induction of MiHDA3 in response to infection of C. gloeosporioides among the 19 tested HDAC genes. Transient overexpression of MiHDA3 in mango fruit strengthened the disease resistance by enhancing the activities of defense-related enzymes (phenylalanine ammonia-lyase (PAL) and β-1,3-glucanase (GLU)) and upregulating the expression levels of MiPAL and MiGLU. These increases occurred concomitantly with increased accumulation of local H₂O₂, a critical signaling molecule. The opposite effects on resistance and H₂O₂ production were observed in MiHDA3-silenced mango fruit. Physiological assays revealed that exogenous H₂O₂ treatment suppressed anthracnose development in mango fruit after inoculation with C. gloeosporioides, whereas treatment with diphenylene iodonium, an inhibitor of endogenous H₂O₂ generation, exacerbated disease symptoms. Furthermore, the mango catalase 1 (MiCAT1), a redox homeostasis-related protein, was confirmed to negatively regulate the resistance of mango fruit to C. gloeosporioides by catalyzing the decomposition of H₂O₂. Mechanistic investigations revealed that MiHDA3-mediated deacetylation of MiCAT1 at lysine residues K227 and K233 reduced the enzymatic activity and protein stability of MiCAT1, contributing to enhanced resistance in mango fruit. Collectively, these findings highlight that the functional interplay between HDACs and catalases can modulate the immune response in post-harvest fruits, and reveal a novel mechanism by which HDACs enhance mango disease resistance through the deacetylation of nonhistone proteins and the regulation of their biochemical functions.