期刊
GENES & DEVELOPMENT
卷 22, 期 11, 页码 1445-1450出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1663208
关键词
Ptf1a; diabetes; endocrine; exocrine; pancreas
资金
- NIDDK NIH HHS [R01 DK075032, U19 DK061245, DK61245, DK75032, DK077480, F32 DK077480, DK56211, R01 DK056211] Funding Source: Medline
The mechanisms regulating pancreatic endocrine versus exocrine fate are not well defined. By analyzing the effects of Ptf1a partial loss of function, we uncovered novel roles for this transcription factor in determining pancreatic fates. In a newly identified hypomorphic ptf1a mutant, pancreatic cells that would normally express ptf1a and become exocrine cells, express the endocrine marker Isl1, indicating a cell fate switch. Surprisingly, a milder reduction of Ptf1a leads to an even greater increase of ectopic endocrine cells, suggesting that Ptf1a also plays a role in promoting endocrine development. We propose that low levels of Ptf1a promote endocrine fate, whereas high levels repress endocrine fate and promote exocrine fate.
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