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Atypical E2f functions are critical for pancreas polyploidization.

Ramadhan B Matondo1, Eva Moreno1, Mathilda J M Toussaint1

  • 1Department of Pathobiology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.

Plos One
|January 13, 2018
PubMed
Summary
This summary is machine-generated.

Atypical E2F transcription factors (E2f7 and E2f8) are essential for pancreatic polyploidization. Their postnatal deletion is compatible with life, revealing new insights into cell regulation and aging.

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Polyploid cells are present in the pancreas, increasing with age in rodents.
  • The molecular regulators and biological functions of pancreatic polyploidization remain largely unknown.

Purpose of the Study:

  • To identify the molecular regulators of pancreatic polyploidization.
  • To investigate the role of atypical E2F transcription factors in this process.

Main Methods:

  • Utilized an inducible Cre/LoxP system in newborn mice to delete E2f7 and E2f8.
  • Analyzed postnatal survival, pancreatic cell ploidy, and serum levels of glucose, insulin, amylase, and lipase.

Main Results:

  • Conditional deletion of both E2f7 and E2f8 in newborn mice suppressed pancreatic polyploidization.
  • Loss of E2f7 or E2f8 alone was sufficient to abolish polyploidization.
  • Mice lacking both atypical E2Fs exhibited normal postnatal survival and lived to old age.
  • Minor decreases in serum glucose, insulin, amylase, and lipase were observed under starvation conditions.

Conclusions:

  • Atypical E2Fs (E2f7 and E2f8) are essential regulators of pancreatic polyploidization.
  • Postnatal loss of atypical E2Fs is compatible with long-term survival.
  • Pancreatic polyploidization does not appear critical for maintaining metabolic homeostasis under normal conditions.