Ribosomal protein genes in post-mortem cortical tissue and iPSC-derived neural progenitor cells are commonly upregulated in expression in autism
Michael Lombardo
Abstract
In a recent paper, Griesi-Oliveira et al. The authors also show proteomic evidence to suggest that these earlier disruptions in translation in NPCs may lead to dysregulation of gene expression relevant to synaptic processes in neurons. These are valuable insights to contribute to the literature, particularly because iPSC models can be a useful model of early prenatal periods of development. also attempted to assess how similar this kind of transcriptomic dysregulation is to previously reported studies using gene expression data in post-mortem cortical tissue. As the authors rightly note, the papers they utilized for this analysis [2, 3] did not themselves report any co-expression modules with differential module eigengene expression in modules enriched for translation processes. However, in our recent paper [4], we re-analyzed data from these studies [2, 3] and indeed identified two consensus co-expression modules enriched in translation processes (M1 and M25) that were replicably upregulated in autism in both datasets. When we examine whether M NPC 10-blue heavily overlaps with these translation-enriched modules, we indeed find high overlap with the translation-enriched M25 coexpression module (odds ratio (OR) = 15.52, p = 1.24e