Atypical E2f functions are critical for pancreas polyploidization

dc.creatorMatondo, RB
dc.creatorMoreno, E
dc.creatorToussaint, MJM
dc.creatorTooten, PCJ
dc.creatorvan Essen, SC
dc.creatorvan Liere, EA
dc.creatorYoussef, SA
dc.creatorBongiovanni, L
dc.creatorde Bruin, A
dc.date2018-10-09T07:52:09Z
dc.date2018-10-09T07:52:09Z
dc.date2018-01-12
dc.date.accessioned2022-10-25T08:50:42Z
dc.date.available2022-10-25T08:50:42Z
dc.descriptionThe 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.
dc.description(NFP grant: R.B.M., DU.282001.1.3.
dc.formatapplication/pdf
dc.identifierhttps://www.suaire.sua.ac.tz/handle/123456789/2617
dc.identifier.urihttp://hdl.handle.net/123456789/90526
dc.languageen
dc.publisherPLOS ONE
dc.subjectE2f8
dc.subjectPancreas
dc.subjectPolyploid
dc.subjectliver
dc.titleAtypical E2f functions are critical for pancreas polyploidization
dc.typeArticle

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