Extended Data Fig. 1: Comparative analysis of protein abundance between PCA-based clustering of HSV iPOND data and whole cell proteome data identifies potential substrates of ICP0. | Nature Microbiology

Extended Data Fig. 1: Comparative analysis of protein abundance between PCA-based clustering of HSV iPOND data and whole cell proteome data identifies potential substrates of ICP0.

From: Comparative proteomics identifies Schlafen 5 (SLFN5) as a herpes simplex virus restriction factor that suppresses viral transcription

Extended Data Fig. 1

a, Venn diagram of PML, ATRX, IFI16, and DNA-PKcs PCA-based clusters identifies proteins that are clustered with each known substrate. b, Volcano plots showing log2 fold change (x-axis) and associated statistical significance (y-axis) for proteins identified by iPOND proteomics, quantifying proteins associated with HSV genomes. Known ICP0 substrates (green) and clustered proteins (blue and red) are indicated. iPOND data comparing HSV WT and ΔICP0 infection shows known substrates and clustered proteins enriched on the ΔICP0 genome. P-values were calculated using the two-tailed unpaired Student’s t-test. n = 3 biologically independent experiments. c, Heatmap showing iPOND abundances as z-scores for mock, WT HSV-1, and ΔICP0 during infection. This list is proteins that are more than 2-fold enriched (dashed gray box in b) on the ΔICP0 virus genome compared to WT HSV-1 genome. These are clustered using a hierarchical clustering algorithm that analyzes the abundance for each condition. Therefore, the proteins with the same trends for mock-HSV-ΔICP0 are close together on the heatmap. d, Whole cell proteome abundance data over a time course of WT HSV-1 infection show decreases in known ICP0 substrates PML, IFI16, and DNA-PKcs, as well as SLFN5. Additional proteins (gray line) showing similar trends in the heat map (c) are not decreased during HSV infection.

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