Sokoine University of Agriculture

Atypical E2f functions are critical for pancreas polyploidization

Show simple item record Matondo, RB Moreno, E Toussaint, MJM Tooten, PCJ van Essen, SC van Liere, EA Youssef, SA Bongiovanni, L de Bruin, A 2018-10-09T07:52:09Z 2018-10-09T07:52:09Z 2018-01-12
dc.description.abstract The presence of polyploid cells in the endocrine and exocrine pancreas has been reported for four decades. In rodents, pancreatic polyploidization is initiated after weaning and the number of polyploid cells increases with age. Surprisingly the molecular regulators and biological functions of polyploidization in the pancreas are still unknown. We discovered that atypical E2f activity is essential for polyploidization in the pancreas, using an inducible Cre/LoxP approach in new-born mice to delete biquitously the atypical E2f transcription factors, E2f7 and E2f8. In contrast to its critical role in embryonic survival, conditional deletion of both of both atypical E2fs in newborn mice had no impact on postnatal survival and mice lived until old age. However, deficiency of E2f7 or E2f8 alone was sufficient to suppress polyploidization in the pancreas and associated with only a minor decrease in blood serum levels of glucose, insulin, amylase and lipase under 4 hours starvation condition compared to wildtype littermates. In mice with fewer pancreatic polyploid cells that were fed ad libitum, no major impact on hormones or enzymes levels was observed. In summary, we identified atypical E2fs to be essential for polyploidization in the pancreas and discovered that postnatal induced loss of both atypical E2fs in many organs is compatible with life until old age. en_US
dc.description.sponsorship (NFP grant: R.B.M., DU.282001.1.3. en_US
dc.language.iso en en_US
dc.publisher PLOS ONE en_US
dc.subject E2f8 en_US
dc.subject Pancreas en_US
dc.subject Polyploid en_US
dc.subject liver en_US
dc.title Atypical E2f functions are critical for pancreas polyploidization en_US
dc.type Article en_US
dc.url en_US

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