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Review
. 2011 Feb;60(2):364-76.
doi: 10.2337/db10-1068.

Historical perspective: beginnings of the beta-cell: current perspectives in beta-cell development

Philip A Seymour  1 , Maike Sander
Affiliations
Review

Historical perspective: beginnings of the beta-cell: current perspectives in beta-cell development

Philip A Seymour et al. Diabetes. 2011 Feb.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Gross morphology of the developing pancreas. Sox9-eGFP demarcates the dorsal pancreatic endoderm (dp) at e9.5 (A) and both dorsal (dp) and ventral (vp) pancreatic buds at e10.5 (B) (embryos shown at same scale). Staining for Pdx1 highlights the epithelium of the pancreatic buds, antral stomach (as), common bile duct (cbd), and duodenum (duo) at e10.5 (C) and e11.5 (D); early glucagon+ endocrine cells differentiate at the periphery of the dorsal pancreatic bud and, following a temporal delay, in the ventral pancreatic bud (z-stack projections shown at same scale). X-Gal staining for lacZ expressed from the Pdx1 locus highlights the dorsal bud-derived (dp) and ventral bud-derived (vp) pancreas, antral stomach (as), common bile duct (cbd), extrahepatic bile ducts (ehd), and duodenum (duo) at e12.5 (E) and e15.5 (F). Gross morphology of the perinatal (e18.5) (G) and adult (four-month-old) (H) pancreas: stom, stomach; spl, spleen. F–H: Pancreas tissue is demarcated by red dashed lines. (A high-quality digital representation of this figure is available in the online issue.)
FIG. 2.
FIG. 2.
Overview of major events in pancreatic morphogenesis. By e10.5, the anlagen of the dorsal (dp) and ventral (vp) pancreas, liver, stomach (stom), and duodenum are established; rapid growth of the pancreatic buds occurs through expansion of the MPC population. From around e11.0 on, neighboring cells undergo cell polarization, generating microlumens with a common apical surface. Over the next few days, microlumen expansion and fusion forms a ductal luminal network; branching morphogenesis of the pancreatic epithelium occurs concordantly with segregation of MPCs by e12.5 into an acinar-committed Ptf1a+ “tip” domain and an Nkx6+ central “trunk” field fated to give rise to the ductal network and endocrine cells. By e15.5, the midpoint of the secondary transition, much acinar cell neogenesis has occurred and the acinar compartment expands predominantly through mitosis. Ngn3+ endocrine progenitor cells delaminate from the Sox9+ Hnf1β+ Muc1+ ductal epithelium and give rise to endocrine cells, which coalesce to form nascent islets.
FIG. 3.
FIG. 3.
Alternative models of endocrine subtype specification from endocrine progenitor cells. Model A: Prevailing model of endocrine subtype specification in wild-type, Arx−/−, Pax4−/−, and compound Arx−/−; Pax4−/− mutants, based on the assumption that cells make binary fate decisions involving an intermediary hypothetical β-/δ-cell precursor cell downstream of Ngn3. Model B: Alternative model in which Arx and Pax4 function to stabilize lineage decisions downstream of Ngn3. Note that PP- and ε-cell populations are excluded for the sake of clarity.
See this image and copyright information in PMC

References

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    1. Kim SK, Hebrok M, Melton DA. Notochord to endoderm signaling is required for pancreas development. Development 1997;124:4243–4252 - PubMed
    1. Kim SK, Melton DA. Pancreas development is promoted by cyclopamine, a hedgehog signaling inhibitor. Proc Natl Acad Sci USA 1998;95:13036–13041 - PMC - PubMed

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