raw Functions through JNK signaling and cadherin-based adhesion to regulate Drosophila gonad morphogenesis.
raw Functions through JNK signaling and cadherin-based adhesion to regulate Drosophila gonad morphogenesis.
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DOI：
10.1016/j.ydbio.2012.04.027
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发表时间：
2012-07-15
影响因子：
2.7
通讯作者：
Van Doren M
中科院分区：
文献类型：
--
作者：
Jemc JC;Milutinovich AB;Weyers JJ;Takeda Y;Van Doren M
为了形成性腺，生殖细胞(GC)和体细胞性腺前体细胞(SGP)必须迁移到发育中的胚胎中的正确位置，并建立必要的细胞-细胞相互作用，以建立适当的性腺结构。在性腺形态发生过程中，SGPS发出细胞突起，包裹单个GC并促进其发育。我们已经确定了原始基因中的突变，这些突变导致SGPS无法包裹GC，从而导致GC发育缺陷。利用遗传分析和基因表达研究，我们发现Raw在性腺形态发生过程中负向调节JNK信号，而JNK信号的增加足以导致包膜缺陷。特别是，Raw在果蝇Jun相关转录因子的上游发挥作用，调节其亚细胞定位。由于JNK信号在许多组织的形态发生过程中调节细胞黏附，我们研究了RAW和编码果蝇E-钙粘蛋白和β-连环蛋白的基因之间的关系，这两个基因在细胞黏附中共同发挥作用。我们发现，DE-钙粘附素的缺失强烈地增强了原始突变性腺的表型，而增加DE-钙粘附素的功能可以挽救这一表型。此外，RAW的丢失会导致？连环蛋白在离开细胞表面时的错误定位。因此，基于钙粘附素的细胞黏附是Raw调节生殖系-胞体相互作用的主要机制。
To form a gonad, germ cells (GCs) and somatic gonadal precursor cells (SGPs) must migrate to the correct location in the developing embryo and establish the cell-cell interactions necessary to create proper gonad architecture. During gonad morphogenesis, SGPs send out cellular extensions to ensheath the individual GCs and promote their development. We have identified mutations in the raw gene that result in a failure of the SGPs to ensheath the GCs, leading to defects in GC development. Using genetic analysis and gene expression studies, we find that Raw negatively regulates JNK signaling during gonad morphogenesis, and increased JNK signaling is sufficient to cause ensheathment defects. In particular, Raw functions upstream of the Drosophila Jun-related transcription factor to regulate its subcellular localization. Since JNK signaling regulates cell adhesion during the morphogenesis of many tissues, we examined the relationship between raw and the genes encoding Drosophila E-cadherin and β-catenin, which function together in cell adhesion. We find that loss of DE-cadherin strongly enhances the raw mutant gonad phenotype, while increasing DE-cadherin function rescues this phenotype. Further, loss of raw results in mislocalization of ß-catenin away from the cell surface. Therefore, cadherin-based cell adhesion, likely at the level of ß-catenin, is a primary mechanism by which Raw regulates germline-soma interaction.
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