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Cell migration that orients the dorsoventral axis is coordinated with anteroposterior patterning mediated by Hedgehog signaling in the early spider embryo.

机译:定向背腹轴的细胞迁移与早期蜘蛛胚胎中的刺猬信号介导的前后模式协调。

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The early embryo of the spider Achaearanea tepidariorum is emerging as a model for the simultaneous study of cell migration and pattern formation. A cell cluster internalized at the center of the radially symmetric germ disc expresses the evolutionarily conserved dorsal signal Decapentaplegic. This cell cluster migrates away from the germ disc center along the basal side of the epithelium to the germ disc rim. This cell migration is thought to be the symmetry-breaking event that establishes the orientation of the dorsoventral axis. In this study, knockdown of a patched homolog, At-ptc, that encodes a putative negative regulator of Hedgehog (Hh) signaling, prevented initiation of the symmetry-breaking cell migration. Knockdown of a smoothened homolog, At-smo, showed that Hh signaling inactivation also arrested the cells at the germ disc center, whereas moderate inactivation resulted in sporadic failure of cell migration termination at the germ disc rim. hh transcript expression patterns indicated that the rim and outside of the germ disc were the source of the Hh ligand. Analyses of patterning events suggested that in the germ disc, short-range Hh signal promotes anterior specification and long-range Hh signal represses caudal specification. Moreover, negative regulation of Hh signaling by At-ptc appears to be required for progressive derepression of caudal specification from the germ disc center. Cell migration defects caused by At-ptc and At-smo knockdown correlated with patterning defects in the germ disc epithelium. We propose that the cell migration crucial for dorsoventral axis orientation in Achaearanea is coordinated with anteroposterior patterning mediated by Hh signaling.
机译:蜘蛛Achaearanea tepidariorum的早期胚胎正在成为同时研究细胞迁移和模式形成的模型。内在径向对称胚盘中心的细胞簇表达了进化保守的背侧信号Decapentaplegic。该细胞簇沿着上皮的基底侧从胚盘中心迁移到胚盘边缘。这种细胞迁移被认为是建立背腹轴方向的对称性破坏事件。在这项研究中,敲除修补的同源物At-ptc的编码(假定编码的刺猬(Hh)信号负调节剂)阻止了破坏对称的细胞迁移的启动。敲除平滑的同源物At-smo表明,Hh信号失活也将细胞停滞在胚盘中心,而中等失活会导致细胞迁移在胚盘边缘的散发失败。 hh转录表达模式表明,胚盘的边缘和外部是Hh配体的来源。对模式事件的分析表明,在胚盘中,短时Hh信号促进前规范,而长时Hh信号抑制尾部规范。此外,似乎需要通过At-ptc对Hh信号进行负调控,以逐步抑制细菌圆盘中心对尾部形态的抑制。由At-ptc和At-smo敲低引起的细胞迁移缺陷与胚盘上皮中的图案缺陷相关。我们建议细胞迁移对于腹足背侧轴方向至关重要的是与Hh信号介导的前后模式协调。

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