Sec61alpha 通过调节 Dpp 信号在果蝇胚胎发生过程中对背侧闭合是必需的。
Sec61alpha is required for dorsal closure during Drosophila embryogenesis through its regulation of Dpp signaling.
机构信息
Department of Molecular Biosciences, University of Kansas, Lawrence, Kansas 66045, USA.
出版信息
Dev Dyn. 2010 Mar;239(3):784-97. doi: 10.1002/dvdy.22219.
Abstract
During dorsal closure in Drosophila, signaling events in the dorsalmost row of epidermal cells (DME cells) direct the migration of lateral epidermal sheets towards the dorsal midline where they fuse to enclose the embryo. A Jun amino-terminal kinase (JNK) cascade in the DME cells induces the expression of Decapentaplegic (Dpp). Dpp signaling then regulates the cytoskeleton in the DME cells and amnioserosa to affect the cell shape changes necessary to complete dorsal closure. We identified a mutation in Sec61alpha that specifically perturbs dorsal closure. Sec61alpha encodes the main subunit of the translocon complex for co-translational import of proteins into the ER. JNK signaling is normal in Sec61alpha mutant embryos, but Dpp signaling is attenuated and the DME cells fail to maintain an actinomyosin cable as epithelial migration fails. Consistent with this model, dorsal closure is rescued in Sec61alpha mutant embryos by an activated form of the Dpp receptor Thick veins.
摘要
在果蝇的背侧闭合过程中，最背侧行的表皮细胞（DME 细胞）中的信号事件指导侧向表皮片向背中线迁移，在那里它们融合以封闭胚胎。DME 细胞中的 Jun 氨基末端激酶（JNK）级联反应诱导 Decapentaplegic（Dpp）的表达。Dpp 信号随后调节 DME 细胞和羊膜中的细胞骨架，以影响完成背侧闭合所需的细胞形状变化。我们鉴定了一个 Sec61alpha 的突变，它专门扰乱了背侧闭合。Sec61alpha 编码用于蛋白质共翻译导入内质网的转位复合物的主要亚基。JNK 信号在 Sec61alpha 突变体胚胎中是正常的，但 Dpp 信号被减弱，DME 细胞不能维持肌动球蛋白电缆，因为上皮迁移失败。与该模型一致的是，Sec61alpha 突变体胚胎中的厚静脉形式的 Dpp 受体的激活形式挽救了背侧闭合。
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