Elevated CO2 regulates the Wnt signaling pathway in mammals, Drosophila melanogaster and Caenorhabditis elegans

Masahiko Shigemura, Emilia Lecuona, Martín Angulo, Laura A. Dada, Melanie B. Edwards, Lynn C. Welch, S. Marina Casalino-Matsuda, Peter H.S. Sporn, István Vadász, Iiro Taneli Helenius, Gustavo A. Nader, Yosef Gruenbaum, Kfir Sharabi, Eoin Cummins, Cormac Taylor, Ankit Bharat, Cara J. Gottardi, Greg J. Beitel, Naftali Kaminski, G. R.Scott BudingerSergejs Berdnikovs, Jacob I. Sznajder*

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

Carbon dioxide (CO2) is sensed by cells and can trigger signals to modify gene expression in different tissues leading to changes in organismal functions. Despite accumulating evidence that several pathways in various organisms are responsive to CO2 elevation (hypercapnia), it has yet to be elucidated how hypercapnia activates genes and signaling pathways, or whether they interact, are integrated, or are conserved across species. Here, we performed a large-scale transcriptomic study to explore the interaction/integration/conservation of hypercapnia-induced genomic responses in mammals (mice and humans) as well as invertebrates (Caenorhabditis elegans and Drosophila melanogaster). We found that hypercapnia activated genes that regulate Wnt signaling in mouse lungs and skeletal muscles in vivo and in several cell lines of different tissue origin. Hypercapnia-responsive Wnt pathway homologues were similarly observed in secondary analysis of available transcriptomic datasets of hypercapnia in a human bronchial cell line, flies and nematodes. Our data suggest the evolutionarily conserved role of high CO2 in regulating Wnt pathway genes.

Original languageEnglish (US)
Article number18251
JournalScientific reports
Volume9
Issue number1
DOIs
StatePublished - Dec 1 2019

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