The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo

Nadin Memar (), Ryan Sherrard, Aditya Sethi, Carla Lloret Fernandez, Henning Schmidt, Eric J. Lambie, Richard J. Poole, Ralf Schnabel and Barbara Conradt ()
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Nadin Memar: University College London
Ryan Sherrard: Ludwig-Maximilians-University Munich
Aditya Sethi: University College London
Carla Lloret Fernandez: University College London
Henning Schmidt: TU Braunschweig
Eric J. Lambie: University College London
Richard J. Poole: University College London
Ralf Schnabel: TU Braunschweig
Barbara Conradt: University College London

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract We report that the eukaryotic replicative helicase CMG (Cdc45-MCM-GINS) is required for differential gene expression in cells produced by asymmetric cell divisions in C. elegans. We found that the C. elegans CMG component, PSF-2 GINS2, is necessary for transcriptional upregulation of the pro-apoptotic gene egl-1 BH3-only that occurs in cells programmed to die after they are produced through asymmetric cell divisions. We propose that CMG’s histone chaperone activity causes epigenetic changes at the egl-1 locus during replication in mother cells, and that these changes are required for egl-1 upregulation in cells programmed to die. We find that PSF-2 is also required for the divergence of other cell fates during C. elegans development, suggesting that this function is not unique to egl-1 expression. Our work uncovers an unexpected role of CMG in cell fate decisions and an intrinsic mechanism for gene expression plasticity in the context of asymmetric cell division.

Date: 2024
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DOI: 10.1038/s41467-024-53715-2

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