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Sec61 α is required for dorsal closure during Drosophila embryogenesis through its regulation of Dpp signaling
Author(s) -
Wang Xiaochen,
Ward Robert E.
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22219
Subject(s) - decapentaplegic , microbiology and biotechnology , biology , embryo , mutant , signal transduction , protein subunit , imaginal disc , genetics , gene
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 Sec61 α that specifically perturbs dorsal closure. Sec61 α encodes the main subunit of the translocon complex for co‐translational import of proteins into the ER. JNK signaling is normal in Sec61 α 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 Sec61 α mutant embryos by an activated form of the Dpp receptor Thick veins. Developmental Dynamics 239:784–797, 2010. © 2010 Wiley‐Liss, Inc.