Transcriptional programs mediating neuronal toxicity and altered glial–neuronal signaling in a Drosophila knock-in tauopathy model

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Figure 4.
Figure 4.

Differential gene expression and enrichment analysis of the scRNA-seq data set in Tau P251L knock-in brains compared with controls. (A) The number of differentially expressed genes (DEGs), both up-regulated and down-regulated genes, in all the annotated clusters of Tau P251L knock-in brains compared with controls. Results are displayed across three major anatomic and functional classes of cells: (1) central body containing three clusters of Kenyon cells (KCs), mushroom body output neurons (MBONs) and pox neurons; (2) optic lobe neurons containing lamina, medullary, and lobula neurons clusters; and (3) glia cells containing astrocytes and perineurial clusters. (B,C) Heatmaps of the top 50 up-regulated (B) and down-regulated (C) genes in all the clusters of Tau P251L knock-in brains compared with controls (Supplemental Table S3). (D) Gene Ontology (GO) enrichment analysis identified top up-regulated and down-regulated biological processes (BPs), molecular functions (MFs), and cellular components (CCs). (E) Analysis of human disease–associated genes revealed top up-regulated and down-regulated disease-associated gene sets. Score represents the combined score c = log(p) × z (Chen et al. 2013).

This Article

  1. Genome Res. 34: 590-605

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