Pdx1, a transcription factor that turns on other genes, is required for the development of the pancreas and for the normal functioning and survival of its insulin-producing beta cells.
Now Maureen Gannon, Ph.D., and colleagues have discovered that Pdx1 doesn’t act alone, at least initially.
Reporting earlier this month in Cell Reports, they describe how a structurally unrelated transcription factor, Oc1, interacts with Pdx1 in multipotent pancreatic progenitor cells to promote endocrine specification and subsequent functional maturation of beta cells.
“It is possible,” the authors write, “that the cooperative activity of Pdx1 and Oc1 in progenitors primes the cells for subsequent steps of the differentiation program.”
This information may be crucial, they conclude, to ongoing efforts to develop a cell-based therapy for diabetes using induced pluripotent stem cells – blood or skin cells removed from patients that have been “reprogrammed” to produce insulin and then returned to them to treat, or cure, their disease.
This research was supported in part by grants from the National Institutes of Health (DK007563, HD000850, DK094723, HD005702, DK089570, DK105689, DK068157, DK089540), the American Heart Association (11PRE7960022), and by a VA Merit Award (1BX000990–01A1).
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