Basic Study
Copyright ©The Author(s) 2025.
World J Gastroenterol. Jul 14, 2025; 31(26): 107044
Published online Jul 14, 2025. doi: 10.3748/wjg.v31.i26.107044
Figure 3
Figure 3 Rotavirus infection enhances Paneth-intestinal stem cells communication. A: Quantification of total inferred cell-cell interactions number and strength between intestinal stem cells in uninfected and infected conditions; B: Differential interaction strength analysis of Paneth cells; C: The stem cell cluster in Figure 1B were re-clustered. Uniform manifold approximation and projection of combined subclustered stem cells from uninfected and infected mice; D: Feature plots (left) and violin plots (right) of the expression of representative marker genes of subclustered stem cells; E: Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of subclustered stem cells; F: Quantification of percent cells per cluster (left) and difference in percent of uninfected and infected cells (right); G: Pseudotime trajectory analysis of stem cells differentiation; H: Ridge plots comparing the differentiation trajectories of stem cells in uninfected (left) and infected (right) conditions. Ctrl: Control; RV: Rotavirus; EEC: Enteroendocrine cell; TA: Transit-amplifying cell; UMAP: Uniform manifold approximation and projection; Lgr5: Leucine-rich repeat-containing G protein-coupled receptor 5; Mki67: Marker of proliferation Ki-67; Olfm4: Olfactomedin 4; Sox4: SRY-related high-mobility-group box 4; Cdk1: Cyclin-dependent kinase 1; Lyz1: Lysozyme 1.