Laboratory for Morphogenetic Signaling, RIKEN Center for Biosystems Dynamics Research, Chuo-ku, Kobe, Hyogo, Japan.
Biosignal Research Center, Kobe University, Nada-ku, Kobe, Hyogo, Japan.
PLoS One. 2018 Dec 21;13(12):e0209058. doi: 10.1371/journal.pone.0209058. eCollection 2018.
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.
昆虫的外表面被角质层覆盖，角质层来源于顶端细胞外基质 (aECM)。aECM 在胚胎发生期间由表皮细胞分泌。aECM 在结构、功能和组成分子上表现出巨大的差异，反映了昆虫外观的巨大多样性。为了研究 aECM 组织和功能的分子原理，我们在这里研究了保守的 aECM 蛋白 ZP 结构域蛋白 Trynity 在黑腹果蝇中的作用。我们首先确定 trynity 是表皮屏障功能所必需的基因。trynity 突变导致角质层最外层包膜层的瓦解，导致小分子渗漏以及生长和蜕皮缺陷。此外，trynity 突变体的气管小管在角质层的孔状结构中出现缺陷，并且突变的气管细胞不能吸收腔蛋白和液体。我们的研究结果表明，trynity 在组织纳米级结构中发挥重要作用，这些结构既限制了分子在表皮中的运输，又促进了气管中的大量吸收脉冲。
