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Pituitary cell translation and secretory capacities are enhanced cell autonomously by the transcription factor Creb3l2

Author

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  • Konstantin Khetchoumian

    (Institut de recherches cliniques de Montréal (IRCM))

  • Aurélio Balsalobre

    (Institut de recherches cliniques de Montréal (IRCM))

  • Alexandre Mayran

    (Institut de recherches cliniques de Montréal (IRCM))

  • Helen Christian

    (University of Oxford)

  • Valérie Chénard

    (McGill University, Rosalind and Morris Goodman Research Centre)

  • Julie St-Pierre

    (McGill University, Rosalind and Morris Goodman Research Centre)

  • Jacques Drouin

    (Institut de recherches cliniques de Montréal (IRCM)
    McGill University, Rosalind and Morris Goodman Research Centre)

Abstract

Translation is a basic cellular process and its capacity is adapted to cell function. In particular, secretory cells achieve high protein synthesis levels without triggering the protein stress response. It is unknown how and when translation capacity is increased during differentiation. Here, we show that the transcription factor Creb3l2 is a scaling factor for translation capacity in pituitary secretory cells and that it directly binds ~75% of regulatory and effector genes for translation. In parallel with this cell-autonomous mechanism, implementation of the physiological UPR pathway prevents triggering the protein stress response. Knockout mice for Tpit, a pituitary differentiation factor, show that Creb3l2 expression and its downstream regulatory network are dependent on Tpit. Further, Creb3l2 acts by direct targeting of translation effector genes in parallel with signaling pathways that otherwise regulate protein synthesis. Expression of Creb3l2 may be a useful means to enhance production of therapeutic proteins.

Suggested Citation

  • Konstantin Khetchoumian & Aurélio Balsalobre & Alexandre Mayran & Helen Christian & Valérie Chénard & Julie St-Pierre & Jacques Drouin, 2019. "Pituitary cell translation and secretory capacities are enhanced cell autonomously by the transcription factor Creb3l2," Nature Communications, Nature, vol. 10(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11894-3
    DOI: 10.1038/s41467-019-11894-3
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    Cited by:

    1. Zhangli Su & Ida Monshaugen & Briana Wilson & Fengbin Wang & Arne Klungland & Rune Ougland & Anindya Dutta, 2022. "TRMT6/61A-dependent base methylation of tRNA-derived fragments regulates gene-silencing activity and the unfolded protein response in bladder cancer," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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