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Selective Filopodia Adhesion Ensures Robust Cell Matching in the Drosophila Heart

机译:选择性氟化肽粘附确保在果蝇心脏中的强大细胞匹配

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摘要

The ability to form specific cell-cell connections within complex cellular environments is critical for multicellular organisms. However, the underlying mechanisms of cell matching that instruct these connections remain elusive. Here, we quantitatively explored the dynamics and regulation of cell matching processes utilizingDrosophilacardiogenesis. We found that cell matching is highly robust at boundaries between cardioblast (CB) subtypes, and filopodia of different CB subtypes have distinct binding affinities. Cdc42 is involved in regulating this selective filopodia binding adhesion and influences CB matching. Further, we identified adhesion molecules Fasciclin III (Fas3) and Ten-m, both of which also regulate synaptic targeting, as having complementary differential expression in CBs. Altering Fas3 expression changes differential filopodia adhesion and leads to?CB mismatch. Furthermore, only when both Fas3?and Ten-m are lost is CB alignment severely impaired. Our results show that differential adhesion mediated by selective filopodia binding efficiently regulates precise and robust cell matching.
机译:在复杂的细胞环境中形成特定细胞间连接的能力对于多细胞生物来说是至关重要的。然而,指示这些连接的细胞匹配的潜在机制仍然难以捉摸。这里,我们定量探索了利用溶质粒细胞发生的细胞匹配过程的动态和调节。我们发现细胞匹配在心血管(Cb)亚型之间的边界处是高度稳健的,并且不同Cb亚型的氟化绦虫具有不同的结合亲和力。 CDC42参与调节这种选择性氟化皮结合粘附性并影响CB匹配。此外,我们鉴定了粘合分子粘性分子筋膜III(FAS3)和十分之一,两者也调节突触靶向,与CBS中具有互补的差异表达。改变FAS3表达改变差分箔粘附性并导致ΔCB不匹配。此外,只有在FAS3和10米都丢失时,只有CB对准严重受损。我们的研究结果表明,通过选择性氟化胶质型结合介导的差异粘附有效地调节精确和强大的细胞匹配。

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