Building a safe space for stem cells: The meristem, the collection of stem cells that builds plants, is resistant to viral infection. Wu et al. now show that WUSCHEL, a transcription factor that helps to sustain stem cell production in the shoot apical meristem of Arabidopsis , also protects that stem cell domain from viruses. WUSCHEL inhibited viral protein synthesis by repressing methyltransferases that regulate ribosomal RNA processing and ribosome stability. Science , this issue p. 227

The ERECTA family genes, ERECTA (ER), ERECTA-LIKE1 (ERL1), and ERECTA-LIKE2 (ERL2), encode leucine-rich repeat receptor-like kinases in Arabidopsis thaliana. Knocking out these three genes can cause severe phenotypes, which indicates that they play significant roles in plant growth and development. However, the molecular mechanism within remains unclear. Here we show that the short hypocotyl phenotypes of er erl1 erl2 mutants are mainly due to the defects of cell elongation rather than the cell division. In contrast, in the ERECTA overexpression transgenic plants, the hypocotyl length is increased with elongated cells. Moreover, we show that the er erl1 erl2 triple mutant contains a low level of auxin, and the expression levels of the key auxin biosynthesis genes are significantly reduced. Consistent with this observation, increasing exogenous or endogenous auxin levels could partially rescue the cell elongation defects of the er erl1 erl2 triple mutant. Therefore, our results provide a molecular basis for auxin mediated ERECTA control of the hypocotyl length in Arabidopsis thaliana.

We investigate the role and mechanism of imbalance via Th9 cells and Th17/Treg cells in the inflammatory and fibrotic phases of pulmonary fibrosis in mice. A total of mice were split into normal saline (control group) and inflammation and fibrosis mouse models (study group) randomly, and lung tissues and bronchoalveolar lavage fluid (BALF) were obtained from mice at the inflammatory and fibrotic phases on the 7th and 28th day, respectively. The degenerative changes in the mouse lung tissue were then visible using H&E staining. The expression of CCR6 and IL-9 in the lung tissues of two groups was examined through an immunohistochemistry assay. Fluorescence PCR was used to assess the expression of PU.1 mRNA in BALF, and flow cytometry was performed to identify the expression of Th17 and Treg. (1). The level of pulmonary fibrosis and lung inflammation in the research group was significantly higher than in the control group. (2). The expression of Th17, CCR6, IL-9 and PU.1 mRNA was substantially higher (P<0.05) in the research group at different time points; the expression level of Treg cells was considerably lower (P<0.05) in the research group than in the control group. (3). CCR6, IL-9 and PU.1 mRNA levels were statistically directly associated (P<0.05) with Th17 and inversely correlated 40 with Regulatory T cells (Tregs). CCR6 and Th9 cells may be involved in 45 developing Th17/Treg imbalance in the immune inflammation of pulmonary fibrosis, which promotes fibrocyte proliferation in lung tissue.

The protective effects of Lactobacillus murinus on chemotherapy-related intestinal injury and immune imbalances were explored by establishing a cyclophosphamide (CTX)-induced mouse model of immunosuppression. CTX treatment led to intestinal barrier destruction, exacerbated local inflammation, and significantly reduced short-chain fatty acid levels (especially butyrate), accompanied by systemic immune suppression. Lactobacillus murinus intervention, especially at medium and high doses, dose-dependently repaired the intestinal barrier, inhibited inflammatory responses, restored levels of metabolites such as butyrate, and systematically regulated splenic immune cell proportions, restoring the CD4⁺/CD8⁺ balance. Metabolomic analysis further revealed that, at different doses, this regulation affected distinct metabolic pathways: low doses enhanced glutathione and purine metabolism, medium doses restored folate and steroid hormone metabolism, and high doses promoted fatty acid β-oxidation and galactose metabolism, forming a multi-level metabolic protective network. This suggests that L. murinus can alleviate chemotherapy-induced intestinal mucositis and mitigate systemic immune suppression through a dual local anti-inflammatory and systemic immune-regulatory effect, with potential mechanisms related to butyrate-mediated regulation of the “metabolism–immune axis,” providing evidence for probiotic-assisted chemotherapy.

Objectives After an episode of acute pulmonary embolism (APE), activated platelets have the ability to release various bioactive factors that can stimulate both proliferation and migration of pulmonary artery smooth muscle cells (PASMCs). SCUBE1 has been previously reported to engage in platelet-platelet interactions, potentially contributing to the activation of platelets in early onset thrombi. The purpose of this study was to examine the alterations in SCUBE1 expression in PASMCs after APE, as well as understand the mechanism behind these changes. Methods The platelet-rich plasma samples of both APE patients and healthy individuals were collected. A hyperproliferative model of PASMCs was established by using platelet-derived growth factor (PDGF) as a stimulator and various assays were used to investigate how SCUBE1-mediated BMP7 can regulate PDGF-induced PASMC proliferation and migration. Results Elevated level of SCUBE1 were observed in platelet-rich plasma from patients with APE and in PASMCs induced by PDGF. SCUBE1 interference ameliorated PDGF-driven cell proliferation and migration, and also downregulated PCNA expression. Additionally, mechanistic studies demonstrated that SCUBE1 could directly bind to bone morphogenetic protein 7 (BMP7) and enhance BMP7 expression, which completely abolished the impact of SCUBE1 silencing on proliferation and migration ability of PASMCs after PDGF treatment. Conclusion In the PDGF-induced proliferation of PASMCs, the expression of SCUBE1 and BMP7 was upregulated. Silencing of SCUBE1 impeded PDGF-induced proliferation and migration of PASMCs by restraining BMP7.

Stem cells are the origin of the germ line in all multicellular organisms, and their genome stability is crucial for population reproduction. How stem cells avoid transmitting incorrect genetic information to the next generation is a fundamental question in species continuity. Here, we show that, in Arabidopsis thaliana, strict control of protein synthesis in stem cells is essential for plant stem cell fate maintenance. Increasing protein synthesis in stem cells causes an overaccumulation of unfolded/misfolded proteins and impairs stem cell maintenance. We demonstrated that stem cells are hypersensitive to unfolded/misfolded proteins, whose accumulation triggers DNA breaks, resulting in genomic instability in stem cells. Our results provide a potential mechanistic link between proteome fidelity and genome stability in stem cells and demonstrate how plants safeguard genome integrity by inhibiting protein synthesis in stem cells.