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Trynity controls epidermal barrier function and respiratory tube maturation in Drosophila by modulating apical extracellular matrix nano-patterning

机译:色散通过调节顶端细胞外基质纳米模式控制果蝇的表皮屏障功能和呼吸管成熟

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摘要

The outer surface of insects is covered by the cuticle, which is derived from the apical extracellular matrix (aECM). The aECM is secreted by epidermal cells during embryogenesis. The aECM exhibits large variations in structure, function, and constituent molecules, reflecting the enormous diversity in insect appearances. To investigate the molecular principles of aECM organization and function, here we studied the role of a conserved aECM protein, the ZP domain protein Trynity, in Drosophila melanogaster. We first identified trynity as an essential gene for epidermal barrier function. trynity mutation caused disintegration of the outermost envelope layer of the cuticle, resulting in small-molecule leakage and in growth and molting defects. In addition, the tracheal tubules of trynity mutants showed defects in pore-like structures of the cuticle, and the mutant tracheal cells failed to absorb luminal proteins and liquid. Our findings indicated that trynity plays essential roles in organizing nano-level structures in the envelope layer of the cuticle that both restrict molecular trafficking through the epidermis and promote the massive absorption pulse in the trachea.
机译:昆虫的外表面被角质层覆盖,角质层是从顶端细胞外基质(aECM)衍生而来的。在胚发生过程中,表皮细胞分泌出aECM。 aECM在结构,功能和组成分子上表现出很大的差异,反映出昆虫外观的巨大差异。为了研究aECM组织和功能的分子原理,在这里我们研究了果蝇中一个保守的aECM蛋白(ZP域蛋白Trynity)的作用。我们首先确定了色散是表皮屏障功能的必需基因。强度突变导致角质层最外层的包膜层崩解,导致小分子渗漏以及生长和蜕皮缺陷。此外,口气性突变体的气管小管在角质层的孔状结构中显示出缺陷,并且突变体的气管细胞无法吸收管腔蛋白和液体。我们的发现表明,try散在组织表皮包膜层的纳米级结构中起着至关重要的作用,既限制了分子通过表皮的运输,又促进了气管中大量的吸收脉冲。

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