Receptor-Type Guanylyl Cyclase at 76C (Gyc76C) Regulates De Novo Lumen Formation during Drosophila Tracheal Development.
Receptor-Type Guanylyl Cyclase at 76C (Gyc76C) Regulates De Novo Lumen Formation during Drosophila Tracheal Development.
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DOI：
10.1371/journal.pone.0161865
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Patel U
中科院分区：
文献类型：
--
作者：
Myat MM;Patel U
管腔的形成和维持对于重要器官如肺、肾和脉管系统的发育和功能是重要的。在果蝇胚胎气管中，管腔重新形成以将不同的气管分支连接成相互连接的管道网络。在这里，我们确定了一个新的作用，受体类型鸟苷酸环化酶在76 C（Gyc 76 C）从头管腔形成的果蝇气管。我们发现，在胚胎中gyc 76 C或其下游效应蛋白激酶G（PKG）1突变，气管腔断开。gyc 76 C突变体胚胎的背干（DT）细胞迁移相互接触，并完成管腔形成的初始步骤，如E-钙粘蛋白（E-cad）的积累和在管腔形成部位形成肌动蛋白轨道。而gyc 76 C突变体胚胎的肌动蛋白轨道和E-cad接触位点没有成熟形成新的腔，DT腔没有融合。我们还观察到失败的管腔蛋白蠕虫状分泌到新的管腔形成的网站在gyc 76 C突变气管。这些DT管腔形成缺陷伴随着Arf样3 GTd 3（Arl 3）的改变的定位，Arl 3是囊泡-囊泡和囊泡-膜融合的已知调节剂。除了DT管腔缺陷，gyc 76 C突变体终末细胞的管腔比野生型细胞短。这些研究表明，Gyc 76 C和下游PKG依赖性信号传导调节气管DT和终末细胞中的从头管腔形成，最有可能是通过影响Arl 3介导的管腔分泌。
Lumen formation and maintenance are important for the development and function of essential organs such as the lung, kidney and vasculature. In the Drosophila embryonic trachea, lumena form de novo to connect the different tracheal branches into an interconnected network of tubes. Here, we identify a novel role for the receptor type guanylyl cyclase at 76C (Gyc76C) in de novo lumen formation in the Drosophila trachea. We show that in embryos mutant for gyc76C or its downsteam effector protein kinase G (PKG) 1, tracheal lumena are disconnected. Dorsal trunk (DT) cells of gyc76C mutant embryos migrate to contact each other and complete the initial steps of lumen formation, such as the accumulation of E-cadherin (E-cad) and formation of an actin track at the site of lumen formation. However, the actin track and E-cad contact site of gyc76C mutant embryos did not mature to become a new lumen and DT lumena did not fuse. We also observed failure of the luminal protein Vermiform to be secreted into the site of new lumen formation in gyc76C mutant trachea. These DT lumen formation defects were accompanied by altered localization of the Arf-like 3 GTPase (Arl3), a known regulator of vesicle-vesicle and vesicle-membrane fusion. In addition to the DT lumen defect, lumena of gyc76C mutant terminal cells were shorter compared to wild-type cells. These studies show that Gyc76C and downstream PKG-dependent signaling regulate de novo lumen formation in the tracheal DT and terminal cells, most likely by affecting Arl3-mediated luminal secretion.
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影响因子：
16.2
作者：
Klassen, Matthew P.;Wu, Ye E.;Maeder, Celine I.;Nakae, Isei;Cueva, Juan G.;Lehrman, Emily K.;Tada, Minoru;Gengyo-Ando, Keiko;Wang, George J.;Goodman, Miriam;Mitani, Shohei;Kontani, Kenji;Katada, Toshiaki;Shen, Kang
通讯作者：
Shen, Kang
影响因子：
2.4
作者：
Patel U;Davies SA;Myat MM
通讯作者：
Myat MM
影响因子：
25
作者：
Micheva, KD;Buchanan, J;Smith, SJ
通讯作者：
Smith, SJ
影响因子：
4.6
作者：
Chak, Kayam;Kolodkin, Alex L.
通讯作者：
Kolodkin, Alex L.
影响因子：
5.3
作者：
Petrov, Aleksej M.;Giniatullin, Arthur R.;Zefirov, Andrej L.
通讯作者：
Zefirov, Andrej L.