Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin-mediated cell adhesion during Drosophila heart tube lumen formation.
Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin-mediated cell adhesion during Drosophila heart tube lumen formation.
复制标题
DOI：
10.1083/jcb.200804120
复制
发表时间：
2008-07-28
期刊：
影响因子：
--
通讯作者：
Kramer SG
中科院分区：
文献类型：
--
作者：
Santiago-Martínez E;Soplop NH;Patel R;Kramer SG
在果蝇心脏发育过程中，对侧成心细胞（CB）的顶端表面之间形成一个腔。我们发现，狭缝和它的受体回旋（机器人）所需的CB顶端域管腔形成。顶端结构域外的Slit的错误定位导致异位腔形成和细胞连接蛋白E-钙粘蛋白（E-Cad）和Enabled的错误定位，而不破坏整体CB细胞极性。异位管腔形成在robo突变体中被抑制，这表明robo对这一过程的需求。遗传证据表明，Robo和Shotgun（Shg）/E-Cad在调节CB粘附中一起起作用。robo和shg/E-Cad转杂合子具有管腔缺陷。在robo功能丧失或shg/E-Cad功能获得胚胎中，由于CB粘附不当和E-Cad在顶膜处积聚，管腔形成受阻。相比之下，shg/E-Cad功能丧失或robo功能获得由于CB粘附的丧失而阻断管腔形成。我们的数据表明，Slit和Robo通路在管腔形成中作为排斥信号发挥作用，以拮抗E-Cad介导的细胞粘附。
During Drosophila melanogaster heart development, a lumen forms between apical surfaces of contralateral cardioblasts (CBs). We show that Slit and its receptor Roundabout (Robo) are required at CB apical domains for lumen formation. Mislocalization of Slit outside the apical domain causes ectopic lumen formation and the mislocalization of cell junction proteins, E-cadherin (E-Cad) and Enabled, without disrupting overall CB cell polarity. Ectopic lumen formation is suppressed in robo mutants, which indicates robo's requirement for this process. Genetic evidence suggests that Robo and Shotgun (Shg)/E-Cad function together in modulating CB adhesion. robo and shg/E-Cad transheterozygotes have lumen defects. In robo loss-of-function or shg/E-Cad gain-of-function embryos, lumen formation is blocked because of inappropriate CB adhesion and an accumulation of E-Cad at the apical membrane. In contrast, shg/E-Cad loss-of-function or robo gain-of-function blocks lumen formation due to a loss of CB adhesion. Our data show that Slit and Robo pathways function in lumen formation as a repulsive signal to antagonize E-Cad–mediated cell adhesion.
登录
查看更多内容
影响因子：
64.5
作者：
Brose, K;Bland, KS;Kidd, T
通讯作者：
Kidd, T
影响因子：
4.6
作者：
Gates, Julie;Mahaffey, James P.;Peifer, Mark
通讯作者：
Peifer, Mark
影响因子：
21.3
作者：
Rhee, J;Mahfooz, NS;VanBerkum, MFA
通讯作者：
VanBerkum, MFA
影响因子：
2.7
作者：
Oda, H;Tsukita, S
通讯作者：
Tsukita, S
影响因子：
64.5
作者：
Kidd, T;Bland, KS;Goodman, CS
通讯作者：
Goodman, CS