Fig. 1: Full-body single-nucleus transcriptome survey of Yki flies.
From: Hepatic gluconeogenesis and PDK3 upregulation drive cancer cachexia in flies and mice
a, The experimental design for gut tumour induction in flies. b, Representative images of gut tumours and phenotypes of Yki flies at days 2, 5, and 8, and control (Ctrl) flies at day 8. The experiment was repeated three times independently, producing similar results. c, A UMAP visualization of cell clusters of control and Yki flies at days 5 and 8, revealed by snRNA-seq. d,e, Bar plot showing the change in total cell percentage of gut cells (d) and ovary cells (e) between control and Yki flies at days 5 and 8; cell proportions were normalized to each condition. f,g, A scatter plot showing the change in cell proportions (Yki versus Ctrl) at day 5 (f) and day 8 (g) on the x axis, and the number of DEGs, which were defined as having P < 0.05 and absolute log2-transformed fold change > 0.38 on the y axis, calculated by the Wilcoxon rank-sum test. h, FlyPhone analysis was performed to calculate the interaction scores between tumour cells (05_intestinal_stem_cell and 06_enterocyte) and peripheral tissues of various ligand–receptor pairs involved in cell–cell communication, persisting at both days 5 and 8. i, The top 10 pathways between tumour and host tissues identified by FlyPhone. j, GSEA was performed on fat body cells (cluster 13_fat_body), and the top 15 enriched pathways are shown. GeneRatio represents the number of input genes mapped to a given pathway divided by the total number of input genes. Statistical significance was assessed by multiple comparisons using the Benjamini–Hochberg method. KEGG, Kyoto Encyclopedia of Genes and Genomes. See also Extended Data Fig. 1.
