Axial protocadherin (AXPC) regulates cell fate during notochordal morphogenesis.

Axial protocadherin (AXPC) regulates cell fate during notochordal morphogenesis.
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DOI:
10.1002/dvdy.22754
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发表时间:
2011-11
影响因子:
2.5
通讯作者:
Gumbiner, Barry M.
Gumbiner, Barry M.
中科院分区:
生物学3区
文献类型:
--
作者:
Yoder, Michael D.;Gumbiner, Barry M.

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中胚层分化为脊索和体节的过程涉及非成簇的δ-原钙粘蛋白。轴向(AXPC)和近轴(PAPC)原钙粘蛋白表达于早期背中胚层,后来分别细化到发育中的脊索和体节中胚层。PAPC在这一过程中的作用已被广泛研究,但AXPC的作用知之甚少。AXPC的部分敲除导致特定的弯曲轴表型,而更严重的敲除导致脊索形成的损失。这些胚胎不能发育脊索不是由于原肠胚形成过程中细胞粘附变化引起的细胞分选事件,而是这种缺陷通过轴向中胚层特化的丧失而表现出来,而不是一般的中胚层诱导。本研究结果表明,AXPC在脊索形态发生中的功能是通过指导细胞命运决定而不是细胞-细胞粘附。
The separation and specification of mesoderm into the notochord and somites involves members of the non-clustered δ-protocadherins. Axial (AXPC) and paraxial (PAPC) protocadherins are expressed in the early dorsal mesoderm and later become refined to the developing notochordal and somitic mesoderm respectively. The role of PAPC in this process has been studied extensively, but the role of AXPC is poorly understood. Partial knockdown of AXPC causes a specific bent axis phenotype, while more severe knockdown results in the loss of notochord formation. The inability of these embryos to develop a notochord is not due to a cell-sorting event via changes in cell adhesion during gastrulation, but rather this defect is manifested through the loss of axial mesoderm specification, but not general mesoderm induction. The results presented here show that AXPC functions in notochord morphogenesis by directing cell fate decisions rather than cell-cell adhesion.
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