MafB is required for islet beta cell maturation

Isabella Artner, Bruno Blanchi, Jeffrey C Raum, Min Guo, Tomomi Kaneko, Sabine Cordes, Michael Sieweke, Roland Stein

Research output: Contribution to journalArticlepeer-review


Pancreatic endocrine cell differentiation depends on transcription factors that also contribute in adult insulin and glucagon gene expression. Islet cell development was examined in mice lacking MafB, a transcription factor expressed in immature alpha (glucagon(+)) and beta (insulin(+)) cells and capable of activating insulin and glucagon expression in vitro. We observed that MafB(-/-) embryos had reduced numbers of insulin(+) and glucagon(+) cells throughout development, whereas the total number of endocrine cells was unchanged. Moreover, production of insulin(+) cells was delayed until embryonic day (E) 13.5 in mutant mice and coincided with the onset of MafA expression, a MafB-related activator of insulin transcription. MafA expression was only detected in the insulin(+) cell population in MafB mutants, whereas many important regulatory proteins continued to be expressed in insulin(-) beta cells. However, Pdx1, Nkx6.1, and GLUT2 were selectively lost in these insulin-deficient cells between E15.5 and E18.5. MafB appears to directly regulate transcription of these genes, because binding was observed within endogenous control region sequences. These results demonstrate that MafB plays a previously uncharacterized role by regulating transcription of key factors during development that are required for the production of mature alpha and beta cells.

Original languageEnglish
Pages (from-to)3853-8
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number10
Publication statusPublished - 2007 Mar 6
Externally publishedYes

Free keywords

  • Animals
  • Cell Differentiation
  • Glucagon
  • Glucose Transporter Type 2
  • Homeodomain Proteins
  • Insulin
  • Insulin-Secreting Cells
  • MafB Transcription Factor
  • Mice
  • Mice, Transgenic
  • Models, Biological
  • Mutation
  • Time Factors
  • Trans-Activators
  • Transcription, Genetic


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