生命科学最新文献

Cigarette smoke is a leading cause of lung cancer, promoting disease progression through remodeling of the immune microenvironment. This study explores the impact of cigarette smoke exposure on the m⁶A reader YTHDC2, its role in inducing macrophage senescence, and the consequent formation of a tumor-supportive inflammatory niche in lung cancer. Single-cell RNA sequencing of lung cancer tissues revealed an enrichment of senescent macrophages with decreased YTHDC2 expression in smokers compared to non-smokers. In vitro experiments showed that cigarette smoke extract (CSE) suppressed YTHDC2 expression in macrophages, resulting in enhanced cellular senescence, increased secretion of pro-inflammatory cytokines and M2-like polarization. Overexpression of YTHDC2 attenuated macrophage senescence by regulating RPS8, thereby limiting the formation of a tumor-promoting microenvironment. In vivo studies using a cigarette smoke-exposed lung cancer model confirmed the role of YTHDC2 in smoke-induced immune microenvironment modulation and tumor progression. These findings identify YTHDC2 as a critical regulator of smoke-induced macrophage senescence and the tumor-promoting microenvironment, providing a potential therapeutic target for lung cancer in smokers.

In response to necrotrophic fungal pathogens, plants often display quantitative disease resistance (QDR), an immune response with complex genetic determinants. Due to their diversity and small phenotypic effect, the genetic bases of QDR are challenging to characterize. Here, we used genome-wide association mapping in Arabidopsis thaliana natural populations to identify novel determinants of QDR against the fungal pathogen Sclerotinia sclerotiorum. We found that presence–absence polymorphism of the AT4TE56270 Copia transposable element (TE) upstream of the cysteine-rich receptor-like kinase 8 (CRK8) gene is associated with QDR. The presence of the TE associates with higher CRK8 expression in healthy and inoculated plants and increased QDR. The constitutive knockdown of CRK8 reduced QDR, hydrogen peroxide production, and the expression of defense genes upon inoculation. Transcriptome analysis revealed altered defense pathways and salt responses in CRK8 mutants, including impaired glutathione and camalexin biosynthesis, likely contributing to disease susceptibility. Mutants in CRK8 showed altered seed germination on salt, and the absence of AT4TE56270 is associated with enhanced seed germination under salt stress in A. thaliana natural populations. These results reveal a trade-off between salt tolerance and defense against S. sclerotiorum associated with presence–absence polymorphism of a TE.

Chilling is an important abiotic stressor that significantly affects cucumber production. Melatonin (MT) modulates chilling responses by interacting with multiple signalling molecules; however, the molecular link between MT and nitric oxide (NO) in cucumbers under chilling stress remains elusive. Herein, we found prolonged chilling stress induced the accumulation of endogenous NO, whereas overexpression of MT biosynthesis gene N-acetylserotonin methyltransferase (CsASMT), with higher endogenous MT content, significantly increased chilling tolerance of cucumbers with decreased accumulation of NO via upregulation of the relative expression of S-nitrosoglutathione reductase gene (CsGSNOR), accompanied by decreased membrane lipid peroxidation and reactive oxygen species (ROS) accumulation. Moreover, we identified a transcription factor zinc finger of Cucumis sativus 10 (CsZAT10), and found CsZAT10 could directly bind to the promoter of CsGSNOR. Furthermore, we found CsZAT10 overexpression enhanced cucumber chilling resistance by directly activating CsGSNOR expression to mediate NO homoeostasis, whereas the suppression of CsZAT10 obviously decreased the chilling tolerance and CsGSNOR expression in cucumber induced by MT. Overall, our results demonstrate that MT enhances chilling tolerance in cucumber by regulating the CsZAT10-CsGSNOR-NO module.

Cadmium (Cd) is a toxic metal that accumulates in plants to inhibit growth and enters the food chain to harm human health. Although Cd accumulation and tolerance in plants have been extensively analysed, their regulation is less understood. Here, we identify a stress-responsive receptor-like kinase (OsSRK) involved in rice Cd accumulation and tolerance. Our results show that OsSRK expression was strongly induced by Cd treatment. OsSRK overexpression decreased while its silencing or mutations increased both Cd accumulation and Cd-induced leaf chlorosis in rice. OsSRK is a close homologue of MULTIPLE SPOROCYTE 1 (MSP1), which controls sporogenic development with its TAPETUM DETERMINANT1 (TPD1)-LIKE 1 A (OsTDL1A) ligand. OsSRK interacts with OsTDL1B, an OsTDL1A homologue, in both yeast and plant cells. Like OsSRK, expression of OsTDL1B was induced by Cd treatment, and mutations of OsTDL1B enhanced both Cd accumulation and Cd-induced symptoms in rice. These results strongly support that OsTDL1B acts as a ligand for the OsSRK receptor kinase in Cd stress signalling. Comparative transcriptome and proteome profiling support that OsSRK plays a critical role in rice Cd accumulation and tolerance through the regulation of genes in Cd accumulation and oxidative stress responses.

As plants grow taller, increasing conductive pathlength imposes hydraulic resistance, challenging the maintenance of water transport to leaves. While tip-to-base conduit widening along the stem helps mitigate this resistance, theoretical models and empirical data suggest that stem widening alone is insufficient to fully compensate. Here, we explore whether leaf length could contribute to maintaining hydraulic conductance by influencing vessel diameters in the stem. Across a diverse set of angiosperm species, we found that leaf length strongly predicts vessel diameter at the petiole base, and that petiole vessel diameter, in turn, scales positively with vessel diameter at the twig tip. These relationships imply that longer leaves are associated with wider conduits in the stem, potentially boosting stem-wide permeability. Simple fluid dynamic models show that the steep rate of conduit widening in angiosperm leaves plausibly buffers the resistance costs of increased leaf length. Because vessel diameter scales with the fourth power of conductance, modest increases in leaf length, and thus stem conduits, could lower the resistance not buffered by conduit widening in the stem. Leaf length during height growth may serve as a key mechanism in maintaining hydraulic supply, complementing conduit widening in the stem.

LEUNIG (LUG) and LEUNIG_HOMOLOG (LUH) are Groucho/Tup1-type transcriptional co-regulators in Arabidopsis thaliana that act redundantly across multiple developmental and environmental response pathways. Their specific contributions to flower development, however, have remained unclear due to embryonic lethality of double mutants. Here, we show that LUH associates with distinct sets of transcription factors and chromatin-associated proteins in a developmentally dynamic manner. Chromatin occupancy and protein interactions shift from a meristem-focused network during early floral patterning to an organogenesis-oriented state as primordia initiate and expand. Reduced promoter-proximal LUH binding coincides with this proliferative phase, suggesting a transient reconfiguration of LUH activity. By later stages, LUH activity is amplified alongside organ differentiation programs. Together with LUG, LUH modulates gene expression programs that are essential for establishing floral organ patterning. These findings reveal how dynamic co-regulator assemblies contribute to the temporal coordination of growth and spatial pattern formation in Arabidopsis flowers.

Flowering is essential for plants to reach the survival of species and flowering is influenced by many environmental factors. However, trithorax group (TrxG) mediated epigenetic modification mechanisms of Physalis grisea under low temperature on flowering remain largely unknown. Here, we report that TrxG core member ULTRAPETALA1 (PgULT1) inhibits flowering in P. grisea by interacting with Polycomb Group (PcG) member LIKE-HETEROCHROMATIN-PROTEIN 1 (PgLHP1) and transcription factor DNA-BINDING-ONE-FINGER 3.4 (PgDOF3.4) to regulate H3K4me3 and H3K27me3. PgULT1 overexpression delayed flowering, yet flowering was relatively promoted under low temperatures. Similarly, PgDOF3.4 confers delayed flowering by transcribing PgULT1, PgLHP1, and FLOWERING LOCUS C (PgFLC). Protein interaction assays indicated that PgULT1, PgDOF3.4 and PgLHP1 can interact with each other, enhance PgFLC transcription and suppress FLOWERING LOCUS T (PgFT) transcription. Genetic evidence demonstrated that PgULT1 and PgLHP1 inhibit flowering by depositing H3K4me3 and H3K27me3 at the PgFLC and PgFT transcription start sites, respectively. PgULT1, PgDOF3.4 and PgLHP1 expression are suppressed under low temperatures, leading to reduced H3K4me3 and H3K27me3 modifications on PgFLC and PgFT promoters, thereby promoting flowering. Collectively, the functional interactions between epigenetic modifiers and transcription factors reveal a cooperative mechanism between TrxG and PcG to respond to low temperatures and promote flowering in P. grisea.