The genetic program of pancreatic β-cell replication in vivo

Agnes Klochendler, Inbal Caspi, Noa Corem, Maya Moran, Oriel Friedlich, Sharona Elgavish, Yuval Nevo, Aharon Helman, Benjamin Glaser, Amir Eden, Shalev Itzkovitz, Yuval Dor*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

59 Scopus citations

Abstract

The molecular program underlying infrequent replication of pancreatic β-cells remains largely inaccessible. Using transgenic mice expressing green fluorescent protein in cycling cells, we sorted live, replicating β-cells and determined their transcriptome. Replicating β-cells upregulate hundreds of proliferation-related genes, along with many novel putative cell cycle components. Strikingly, genes involved in β-cell functions, namely, glucose sensing and insulin secretion, were repressed. Further studies using single-molecule RNA in situ hybridization revealed that in fact, replicating β-cells double the amount of RNA for most genes, but this upregulation excludes genes involved in β-cell function. These data suggest that the quiescence-proliferation transition involves global amplification of gene expression, except for a subset of tissue-specific genes, which are "left behind" and whose relative mRNA amount decreases. Our work provides a unique resource for the study of replicating β-cells in vivo.

Original languageAmerican English
Pages (from-to)2081-2093
Number of pages13
JournalDiabetes
Volume65
Issue number7
DOIs
StatePublished - 1 Jul 2016

Bibliographical note

Publisher Copyright:
© 2016 by the American Diabetes Association.

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