Planar cell polarity genes regulate polarized extracellular matrix deposition during frog gastrulation

Planar cell polarity genes regulate polarized extracellular matrix deposition during frog gastrulation
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DOI:
10.1016/j.cub.2005.03.040
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发表时间:
2005-04-26
期刊:
影响因子:
9.2
通讯作者:
Keller, R
Keller, R
中科院分区:
生物学1区
文献类型:
--
作者:
Goto, T;Davidson, L;Keller, R

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非典型的 wnt/平面细胞极性 (PCP) 通路 [1] 调节中间(平面)极化细胞的突出活动和嵌入,驱动脊椎动物原肠胚形成的会聚伸展运动 [2],但其潜在机制尚不清楚。我们报告了非洲爪蟾 PCP 基因斜视 (Xstbm)、卷曲 (Xfz7) 和 Prickle (Xpk) 的扰动表达,破坏了中胚层组织表面上的径向极化纤连蛋白原纤维组装、中外侧极化运动和嵌入。极化运动在 Xpk 扰动的外植体中恢复,但在纤连蛋白表面培养的 Xstbm 或 Xfz7 扰动的外植体中没有恢复。 PCP 复合物(包括 Xpk)首先调节纤连蛋白基质的极化表面组装,这对于内侧极化运动是必需的,然后,如果没有 Xpk,则在极化运动中具有额外且必要的功能。这些结果表明,PCP 复合物通过间接和直接机制调节多种细胞极性(径向、平面)和多种过程(基质沉积、运动),并在脊椎动物形态发生过程中以其全部或部分成分以多种模式发挥作用。
The noncanonical wnt/planar cell polarity (PCP) pathway [1] regulates the mediolaterally (planarly) polarized cell protrusive activity and intercalation that drives the convergent extension movements of vertebrate gastrulation [2], yet the underlying mechanism is unknown. We report that perturbing expression of Xenopus PCP genes, Strabismus (Xstbm), Frizzled (Xfz7), and Prickle (Xpk), disrupts radially polarized fibronectin fibril assembly on mesodermal tissue surfaces, mediolaterally polarized motility, and intercalation. Polarized motility is restored in Xpk-perturbed explants but not in Xstbm- or Xfz7-perturbed explants cultured on fibronectin surfaces. The PCP complex, including Xpk, first regulates polarized surface assembly of the fibronectin matrix, which is necessary for mediolaterally polarized motility, and then, without Xpk, has an additional and necessary function in polarizing motility. These results show that the PCP complex regulates several cell polarities (radial, planar) and several processes (matrix deposition, motility), by indirect and direct mechanisms, and acts in several modes, either with all or a subset of its components, during vertebrate morphogenesis.