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Calcium (Ca) deficiency symptoms, such as blossom end rot in tomato and tip burn in lettuce, are among the most serious physiological disorders in agriculture. A common feature of this disorder is the expansion of necrosis. However, mechanisms underlying Ca-deficiency-induced necrosis remain poorly understood. We previously identified callose synthase genes (GSL1, GSL8, GSL10) as the causal genes of low-Ca-sensitive Arabidopsis thaliana mutants, which exhibit severe cell death in true leaves and reduced callose accumulation in cotyledons under low-Ca conditions. This raises the question of whether callose accumulation suppresses the spread of cell death. To clarify their relationship within the same organ, we examined callose deposition and cell death in the cotyledons of the gsl10 mutant. Although the gsl10 mutant showed a comparable level of total cell death to wild-type plants, the necrotic spots were larger. Furthermore, the largest necrotic spots were typically found at the cotyledon tip, but this tendency was weaker in gsl10 mutant. Collectively, our results suggest that callose does not suppress the initiation of cell death but rather limits its propagation, thereby leading to the formation of a characteristic necrotic pattern preferentially occurring at the cotyledon tip.

NF-YA1 (nuclear factor Y, subunit A1) is a key transcription factor that participates in the regulation of plant growth and stress responses. In plants, NF-YA proteins are encoded by multigene families and play crucial roles in controlling gene expression related to development, metabolism, and adaptation to environmental constraints. Therefore, NF-YA transcription factors are considered promising targets for improving plant tolerance to abiotic stress. In our previous study, we demonstrated that TdNF-YA2A-1 transcripts from durum wheat are induced by various abiotic stressors, and that heterologous expression of this gene enhances stress tolerance in yeast. Herein, we functionally investigated its role in transgenic tobacco. RT-qPCR analysis demonstrated that TdNF-YA2A-1 expression was differentially regulated in durum wheat tissues subjected to salt (150  mM NaCl), osmotic (10% PEG 8000), and oxidative (10 µM H₂O₂) stresses. Transgenic TdNFY-YA2A-1-overexpressing tobacco lines exhibited enhanced tolerance to both salt and osmotic stress relative with non-transgenic (NT) plants. This enhanced tolerance was correlated with a reduction in oxidative damage and the upregulation of several stress-responsive genes involved in antioxidant defense and stress signaling. Taken together, our results suggest that TdNF-YA2A-1 is a promising candidate gene for developing crops with improved tolerance to salt and osmotic stresses.

Rice yield is directly influenced by spikelet number, a trait governed by both genetic and hormonal regulatory pathways. In this study, we demonstrate that GNA, a GRAS family transcription factor, acts as a key positive regulator of spikelet development in rice. Through map-based cloning, transgenic manipulation, and molecular assays, we show that GNA enhances grain number per panicle by repressing OsCKX2, a cytokinin oxidase gene responsible for cytokinin degradation. Chromatin immunoprecipitation, luciferase activity assays, and electrophoretic mobility shift assays (EMSA) confirm that GNA directly binds to the OsCKX2 promoter, suppressing its transcription and thereby elevating endogenous cytokinin levels. Notably, GNA physically interacts with DEP1/dep1, and this interaction further enhances the GNA-mediated repression of OsCKX2. Overexpression of GNA significantly increases spikelet number, pedicel branching, and grain yield per plant, accompanied by the activation of cytokinin-responsive genes. These findings reveal a previously uncharacterized DEP1-GNA-OsCKX2 regulatory module that links G-protein signaling with cytokinin signaling and panicle morphogenesis, providing a promising genetic target for rice yield improvement and molecular breeding.

Nuclear trafficking is essential for cellular function and biomedical applications such as nucleus-targeted drug delivery; however, how passive nuclear transport varies across cell types and phenotypic states remains poorly understood. Here, we investigate passive nuclear transport of fluorescent molecular cargoes spanning 500-20,000 Da across multiple cell lines. We observe cell-line-specific nuclear restrictions and find that passive nuclear uptake does not exhibit a monotonic dependence on molecular weight, suggesting non-Fickian transport behavior. Furthermore, transforming a healthy breast cell model into an invasive-like phenotype via TGF-Beta treatment significantly altered passive nuclear transport characteristics, closely resembling those of a well-established invasive breast cancer cell line. These phenotype-dependent changes in nuclear permeability provide new insight into fundamental biophysical alterations associated with cancerous cellular transformation.

Progress toward Universal Health Coverage (UHC) remains a priority for low- and middle-income countries (LMICs). For countries that have adopted Social Health Insurance (SHI) as a strategy, expanding coverage among informal sector households presents an important pathway to this goal. This scoping review examines strategies and interventions employed in LMICs to improve the enrollment and retention of informal sector households in SHI schemes. The review highlights common barriers, including irregular incomes, limited awareness, administrative challenges, and trust deficits. Potential strategies include designing flexible contribution mechanisms, simplified registration processes, targeted awareness campaigns, leveraging existing community structures, and designing comprehensive benefit packages that balance coverage goals with fiscal sustainability. Our findings emphasize the importance of context-specific and innovative approaches that could include tiered premiums, mobile payment platforms, and partnerships with microfinance institutions to address financial and logistical barriers. However, there is also evidence to suggest that net revenue gains from contributory mechanisms are typically modest, with enrollment expansion often requiring substantial public subsidies and incurring additional administrative costs. For Zambia, integrating some of these lessons into the National Health Insurance Scheme (NHIS) offers a pathway to enhancing coverage among the informal sector and advancing equitable access to healthcare, while acknowledging the fiscal constraints.

Brassinosteroid (BR)-mediated salt tolerance is a crucial mechanism for maize (Zea mays L.) adaptation to saline-alkaline environments. This study aimed to elucidate the molecular mechanism underlying BR-induced salt tolerance in maize, focusing on the regulatory roles of ZmWRKY104 and ZmCCaMK. Key results showed that ZmWRKY104 directly interacts with ZmCCaMK in the nucleus in a non-phosphorylation-dependent manner, forming a novel regulatory module. BR treatment upregulates ZmWRKY104 expression, and overexpression of ZmWRKY104 significantly enhances the activities of antioxidant enzymes (APX and SOD). Co-expression of ZmWRKY104 and ZmCCaMK synergistically promotes the antioxidant defense system in maize. Transgenic maize overexpressing ZmWRKY104 exhibits obvious salt tolerance advantages under 100 mM NaCl stress compared to wild-type plants, including reduced leaf yellowing, increased plant height and root length, as well as decreased electrolyte leakage (EL) and malondialdehyde (MDA) content. Collectively, this study identifies a novel non-phosphorylation-dependent WRKY-CCaMK regulatory module in the BR signaling pathway, which enhances BR-induced maize salt tolerance by synergistically activating antioxidant defense. The findings highlight ZmWRKY104 as a candidate gene and provide a potential molecular mechanism for salt-tolerant maize breeding in saline-alkaline regions of northern China.

This study investigates how brassinosteroids (BRs) enhance stress tolerance in soybean under combined salt and drought stress by examining growth, chlorophyll content, photosynthesis, and reactive oxygen species (ROS) homeostasis. Salt and drought stress significantly reduced soybean growth and photosynthetic performance, as reflected by lower SPAD chlorophyll values and decreased photosystem II (PSII) efficiency. In contrast, BR (24-epibrassinolide, EBL) significantly improved growth parameters and spectral indices, indicating a healthier pigment status and improved canopy function. EBL-treated plants also exhibited enhanced PSII performance, as indicated by increased Fv/Fm and a higher performance index (PI). Furthermore, BRs modulated ROS levels and promoted cellular homeostasis by elevating the activities of antioxidant enzymes such as APX, CAT, and POX, thereby mitigating oxidative damage. Consistently, expression of key stress-responsive genes (GmCAT, GmSOD, and GmP5CS) was strongly induced under combined salt, drought, and EBL treatment, highlighting the synergistic role of EBL in transcriptional activation under combined stress. EBL treatment increased the proline content and the activities of ProDH and P5CS, supporting proline-mediated osmoprotection, while BR-treated plants exhibited reduced malondialdehyde (MDA) accumulation and electrolyte leakage (EL), indicating lower lipid peroxidation and better membrane integrity under stress. Overall, this study demonstrates that EBL enhances soybean resilience to combined salt and drought stress by improving growth, photosynthetic efficiency, antioxidant defense, osmotic adjustment, and membrane stability.

The CASEIN KINASE 1 (CK1) family plays diverse roles in the development, physiology, and disease in eukaryotes. In Arabidopsis thaliana, the CASEIN KINASE 1-LIKE (CKL) family has 13 members, but to date, the roles of these kinases remain largely unclear. Here, we characterize several insertion mutants, finding that CKL12 may contribute to hypocotyl and primary root growth. Differential effects of insertions at various parts of the gene suggest that the 3' end of the transcript may be important for CKL12 function. We provide evidence that CKL12 may be a transcriptional target of brassinosteroid (BR) signaling. The CKL12 promoter contains in vitro binding sites for BR-related transcription factors. Knock-down of these transcription factors using RNA interference reduces CKL12 transcript. Together, these data suggest that CKL12 may act downstream of BR signaling to regulate seedling growth.

Flood-induced hypoxia (low oxygen concentration) is increasing in frequency and intensity due to climate change, leading to significant crop yield losses and posing a major threat to global food security. S-nitrosoglutathione reductase (GSNOR) is a highly conserved, cysteine-rich homodimer that regulates the cellular level of the most abundant nitric oxide (NO) reservoir S-nitrosoglutathione (GSNO). GSNOR plays a fundamental role in NO homeostasis, as well as in plant development and stress responses, particularly hypoxia. This review summarizes the critical position of GSNOR in the plant hypoxia regulation network. We discuss how GSNOR controls the intracellular pool of S-nitrosothiols (SNOs), especially GSNO, thereby mitigating cytotoxic nitrosative stress while fine-tuning NO-mediated posttranslational modifications (PTMs), such as S-nitrosylation. Furthermore, we explored the regulation of GSNOR activity through various mechanisms, including oxidative PTMs and protein‒protein interactions. Targeted manipulation of GSNOR activity represents a promising strategy for enhancing flood tolerance in agriculturally important crops. We propose possible approaches for GSNOR manipulation and highlight urgent questions that must be addressed in future research to improve flood resilience in agricultural systems and protect global food security.