Extensive elimination of acinar cells during normal postnatal pancreas growth

Miri Stolovich-Rain, Ori Fridlich, Shira Azulai, Agnes Klochendler, Shira Anzi, Judith Magenheim, Ilan Stein, Fatima Mushasha, Benjamin Glaser, Eli Pikarsky, Danny Ben-Zvi, Yuval Dor*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


While programmed cell death plays important roles during morphogenetic stages of development, post-differentiation organ growth is considered an efficient process whereby cell proliferation increases cell number. Here we demonstrate that early postnatal growth of the pancreas unexpectedly involves massive acinar cell elimination. Measurements of cell proliferation and death in the human pancreas in comparison to the actual increase in cell number predict daily elimination of 0.7% of cells, offsetting 88% of cell formation over the first year of life. Using mouse models, we show that death is associated with mitosis, through a failure of dividing cells to generate two viable daughters. In p53-deficient mice, acinar cell death and proliferation are reduced, while organ size is normal, suggesting that p53-dependent developmental apoptosis triggers compensatory proliferation. We propose that excess cell turnover during growth of the pancreas, and presumably other organs, facilitates robustness to perturbations and supports maintenance of tissue architecture.

Original languageAmerican English
Article number113457
JournalCell Reports
Issue number12
StatePublished - 26 Dec 2023

Bibliographical note

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  • CP: Developmental biology
  • acinar cells
  • compensatory proliferation
  • p53
  • pancreas
  • postnatal development
  • programmed cell death


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