Bioinformatics analysis showing that α-actinin-1 deficiency alters platelet production and function through mitochondrial protein expression. (A) Heat map of the MK proteomics of low (ploidy 2 N and 4 N) or high (ploidy ≥8 N) ploidy after differential protein expression analysis. (B) Volcano plots showing differential protein expression in low- or high-ploidy MKs between Actn1f/f and PF4-Actn1−/− mice. (C) GSEA of differentially expressed proteins in high-ploidy MKs between Actn1f/f and PF4-Actn1−/− mice. The altered proteins in high-ploidy MKs revealed a signature related to platelet activation signaling and aggregation and mitochondria. (D) Network of enriched terms, which are colored according to cluster identity (ID), with nodes that share the same cluster ID typically close to each other. (E) Volcano plot of differential protein expression in platelets between Actn1f/f and PF4-Actn1−/− mice. (F) GSEA of differentially expressed proteins in platelets from Actn1f/f and PF4-Actn1−/− mice. The altered proteins in platelets revealed a signature related to factors involved in MK development and platelet production and adherens junction interactions. (G) Volcano plot of differentially expressed genes in MKs between Actn1f/f and PF4-Actn1−/− mice. GO, gene ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes.
