Preprint Article Version 1 This version is not peer-reviewed

Oligodendrocytes Remodel the Genomic Fabrics of Functional Pathways in Astrocytes

Version 1 : Received: 3 April 2020 / Approved: 6 April 2020 / Online: 6 April 2020 (12:36:20 CEST)

A peer-reviewed article of this Preprint also exists.

Iacobas, D.A.; Iacobas, S.; Stout, R.F.; Spray, D.C. Cellular Environment Remodels the Genomic Fabrics of Functional Pathways in Astrocytes. Genes 2020, 11, 520. Iacobas, D.A.; Iacobas, S.; Stout, R.F.; Spray, D.C. Cellular Environment Remodels the Genomic Fabrics of Functional Pathways in Astrocytes. Genes 2020, 11, 520.

Journal reference: Genes 2020, 11, 520
DOI: 10.3390/genes11050520

Abstract

We profiled the transcriptomes of primary mouse cortical astrocytes cultured alone or co-cultured with immortalized precursor oligodendrocytes. The experimental set-up (insert systems) prevented formation of gap junction channels but allowed free exchange of the two culture media. The study complements our previously published reports that the genomic fabrics of major functional pathways in oligodendrocytes are substantially remodeled by the proximity of non-touching astrocytes. Here, we present new analysis indicating that the transcriptomic landscape of astrocytes likewise changes significantly in the proximity of non-touching oligodendrocytes. The research was stimulated by the reported transcriptomic similarity between the brains of Cx43KO and Cx32KO mice, both substantially different from that of the Cx36KO mice. Since the three connexins are expressed in different cell types (Cx43 in astrocytes, Cx32 in oligodendrocytes and Cx36 in neurons), altogether these findings support the idea of a “panglial transcriptomic syncytium” in the mouse brain. Going further, our results suggest that integration in a heterocellular tissue modulates not only the expression profile but also the expression control and networking of the genes in each cell phenotype.

Subject Areas

calcium signaling; chemokine signaling; gap junction; NOD-like receptor signaling; oli-neu cells; pannexin1; PI3K-Akt pathway; thyroid hormone pathway

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