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

Author

Listed:
  • Nadin Memar

    (University College London
    Institute for Basic Science (IBS))

  • 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)

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.

Suggested Citation

  • Nadin Memar & Ryan Sherrard & Aditya Sethi & Carla Lloret Fernandez & Henning Schmidt & Eric J. Lambie & Richard J. Poole & Ralf Schnabel & Barbara Conradt, 2024. "The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-53715-2
    DOI: 10.1038/s41467-024-53715-2
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    References listed on IDEAS

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    1. Daniel J. Hoeppner & Michael O. Hengartner & Ralf Schnabel, 2001. "Engulfment genes cooperate with ced-3 to promote cell death in Caenorhabditis elegans," Nature, Nature, vol. 412(6843), pages 202-206, July.
    2. Peter W. Reddien & Scott Cameron & H. Robert Horvitz, 2001. "Phagocytosis promotes programmed cell death in C. elegans," Nature, Nature, vol. 412(6843), pages 198-202, July.
    3. Zhiming Li & Shoufu Duan & Xu Hua & Xiaowei Xu & Yinglu Li & Demis Menolfi & Hui Zhou & Chao Lu & Shan Zha & Stephen P. Goff & Zhiguo Zhang, 2023. "Asymmetric distribution of parental H3K9me3 in S phase silences L1 elements," Nature, Nature, vol. 623(7987), pages 643-651, November.
    4. Sayantan Chakraborty & Eric J. Lambie & Samik Bindu & Tamara Mikeladze-Dvali & Barbara Conradt, 2015. "Engulfment pathways promote programmed cell death by enhancing the unequal segregation of apoptotic potential," Nature Communications, Nature, vol. 6(1), pages 1-9, December.
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