Tubular endocytosis drives remodelling of the apical surface during epithelial morphogenesis in Drosophila.
Tubular endocytosis drives remodelling of the apical surface during epithelial morphogenesis in Drosophila.
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DOI：
10.1038/ncomms3244
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发表时间：
2013
影响因子：
16.6
通讯作者：
De Renzis, Stefano
中科院分区：
文献类型：
--
作者：
Fabrowski, Piotr;Necakov, Aleksandar S.;Mumbauer, Simone;Loeser, Eva;Reversi, Alessandra;Streichan, Sebastian;Briggs, John A. G.;De Renzis, Stefano
在形态发生过程中，细胞形状的重塑需要质膜结构域的扩张或收缩。在这里，我们确定了一种机制，在果蝇上皮形态发生的顶端表面的重组。我们发现，绒毛突起的回缩和随后的顶端质膜变平是一个内吞驱动的形态发生过程。内源标记的GFP：：Rab 5动力学的定量揭示了与顶端形态学变化相关的顶端内吞作用的大量增加。这种增加伴随着管状质膜内陷的形成，其作为Rab 5阳性内体从头产生的平台。我们确定Rab 5效应Rabankyrin-5作为该途径的调节剂，并证明阻断发动蛋白活性导致肾小管内吞作用的完全抑制，Rab 5内体的消失，以及表面平坦化的抑制。这些数据共同证明了上皮发育过程中形态发生重塑中的内吞作用的要求。 在果蝇的上皮形态发生过程中，绒毛顶端细胞表面是扁平的。Fabrowski等人表明，这种扁平化依赖于与小管内陷形成相关的内吞作用的急剧增加，揭示了膜运输在形态重塑中的作用。
During morphogenesis, remodelling of cell shape requires the expansion or contraction of plasma membrane domains. Here we identify a mechanism underlying the restructuring of the apical surface during epithelial morphogenesis in Drosophila. We show that the retraction of villous protrusions and subsequent apical plasma membrane flattening is an endocytosis-driven morphogenetic process. Quantitation of endogenously tagged GFP::Rab5 dynamics reveals a massive increase in apical endocytosis that correlates with changes in apical morphology. This increase is accompanied by the formation of tubular plasma membrane invaginations that serve as platforms for the de novo generation of Rab5-positive endosomes. We identify the Rab5-effector Rabankyrin-5 as a regulator of this pathway and demonstrate that blocking dynamin activity results in the complete inhibition of tubular endocytosis, in the disappearance of Rab5 endosomes, and in the inhibition of surface flattening. These data collectively demonstrate a requirement for endocytosis in morphogenetic remodelling during epithelial development. During epithelial morphogenesis in Drosophila, the villous apical cell surface is flattened. Fabrowski et al. show that this flattening depends on a dramatic increase in endocytosis associated with the formation of tubular invaginations, revealing a role for membrane trafficking in morphological remodelling.
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