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Autophagy repurposes cells during paligenosis.

Zhi-Feng Miao1,2, Charles J Cho1, Zhen-Ning Wang2

  • 1Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.

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Summary

Paligenosis allows differentiated cells to revert to a stem-like state for tissue repair. Key genes DDIT4 and IFRD1 regulate this process by controlling MTORC1 activity and cell cycle reentry.

Keywords:
Acinar-ductal metaplasia (ADM)dedifferentiationprogenitor cellregenerationspasmolytic polypeptide-expressing metaplasia (SPEM)tumorigenesis

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Differentiated cells can dedifferentiate to a stem or progenitor state through paligenosis to enable tissue repair.
  • Paligenosis involves sequential stages: MTORC1 quenching and autophagy, progenitor gene induction, and MTORC1 reactivation for cell cycle reentry.

Purpose of the Study:

  • To summarize research on the critical regulators of paligenosis, focusing on evolutionarily conserved genes.
  • To elucidate the roles of DDIT4 and IFRD1 in controlling the stages of paligenosis.

Main Methods:

  • Review of existing research on paligenosis and its genetic regulation.
  • Analysis of the functions of DDIT4 and IFRD1 in MTORC1 signaling and cell cycle control during paligenosis.

Main Results:

  • DDIT4 suppresses MTORC1 activity, promoting autophagy and lysosome formation in the first stage of paligenosis.
  • IFRD1 facilitates cell cycle reentry by suppressing TRP53, which maintains MTORC1 suppression.
  • TRP53 remains active in cells with DNA damage, preventing cell cycle reentry until repair or apoptosis.

Conclusions:

  • DDIT4 and IFRD1 are essential regulators of paligenosis, orchestrating the transition from differentiated cells to a progenitor state.
  • Understanding paligenosis and its dedicated genes offers novel strategies for enhancing tissue regeneration and targeting cancer cells.