development 2篇

flydayzhu

http://dev.biologists.org/conten ... 33.abstract?papetoc
7 I' `& Y+ }- |2 Q' C0 |A Sox9/Fgf feed-forward loop maintains pancreatic organ identity
% E0 B; {* a/ w- \2 G2 p. r7 lPhilip A. Seymour, Hung Ping Shih, Nisha A. Patel, Kristine K. Freude, Ruiyu Xie, Christopher J. Lim and Maike Sander*
! V, m, b: w- V  Y' P5 `) C↵*Author for correspondence: masander@ucsd.edu/ Y, h: r- c, q$ `; P: f/ l
Summary
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All mature pancreatic cell types arise from organ-specific multipotent progenitor cells. Although previous studies have identified cell-intrinsic and -extrinsic cues for progenitor cell expansion, it is unclear how these cues are integrated within the niche of the developing organ. Here, we present genetic evidence in mice that the transcription factor Sox9 forms the centerpiece of a gene regulatory network that is crucial for proper organ growth and maintenance of organ identity. We show that pancreatic progenitor-specific ablation of Sox9 during early pancreas development causes pancreas-to-liver cell fate conversion. Sox9 deficiency results in cell-autonomous loss of the fibroblast growth factor receptor (Fgfr) 2b, which is required for transducing mesenchymal Fgf10 signals. Likewise, Fgf10 is required to maintain expression of Sox9 and Fgfr2 in epithelial progenitors, showing that Sox9, Fgfr2 and Fgf10 form a feed-forward expression loop in the early pancreatic organ niche. Mirroring Sox9 deficiency, perturbation of Fgfr signaling in pancreatic explants or genetic inactivation of Fgf10 also result in hepatic cell fate conversion. Combined with previous findings that Fgfr2b or Fgf10 are necessary for pancreatic progenitor cell proliferation, our results demonstrate that organ fate commitment and progenitor cell expansion are coordinately controlled by the activity of a Sox9/Fgf10/Fgfr2b feed-forward loop in the pancreatic niche. This self-promoting Sox9/Fgf10/Fgfr2b loop may regulate cell identity and organ size in a broad spectrum of developmental and regenerative contexts.
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$ E% s4 r( C8 Mhttp://dev.biologists.org/content/139/16/2833.abstract3 B( v" i% `; A; k

3 E% o0 l) R& J& hVascular instruction of pancreas development6 h# T1 h* k) I  P5 }
Ondine Cleaver1,* and Yuval Dor2
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1 Department of Molecular Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.- _$ e* t3 ^; V, D# }1 o6 S
2 Department of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel.
# e: E6 S0 x9 X, a" t↵* Author for correspondence (ondine.cleaver@utsouthwestern.edu)
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, j3 L9 h3 a8 n. {" ?  ?Blood vessels course through organs, providing them with essential nutrient and gaseous exchange. However, the vasculature has also been shown to provide non-nutritional signals that play key roles in the control of organ growth, morphogenesis and homeostasis. Here, we examine a decade of work on the contribution of vascular paracrine signals to developing tissues, with a focus on pancreatic β-cells. During the early stages of embryonic development, blood vessels are required for pancreas specification. Later, the vasculature constrains pancreas branching, differentiation and growth. During adult life, capillaries provide a vascular niche for the maintenance of β-cell function and survival. We explore the possibility that the vasculature constitutes a dynamic and regionalized signaling system that carries out multiple and changing functions as it coordinately grows with the pancreatic epithelial tree.

tsiacai

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莫非白

谢谢楼主，正好也在找后面那篇