ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2010
Sec61alpha is required for dorsal closure during Drosophila embryogenesis through its regulation of Dpp signaling.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Septate junction proteins are required for cell shape changes, actomyosin reorganization and cell adhesion during dorsal closure inFrontiers in cell and developmental biology · 2022Article
- Identifying Key Genetic Regions for Cell Sheet Morphogenesis on Chromosome 2L Using aG3 (Bethesda, Md.) · 2020Article
- Drak Is Required for Actomyosin Organization During Drosophila Cellularization.G3 (Bethesda, Md.) · 2016Article
- Macroglobulin complement-related encodes a protein required for septate junction organization and paracellular barrier function in Drosophila.Development (Cambridge, England) · 2014Article
- Genome-wide RNAi screen identifies SEC61A and VCP as conserved regulators of Sindbis virus entry.Cell reports · 2013Article
- Contribution of Sec61α to the life cycle of Ebola virus.The Journal of infectious diseases · 2011Article
- Distinct tissue distributions and subcellular localizations of differently phosphorylated forms of the myosin regulatory light chain in Drosophila.Gene expression patterns : GEPArticle
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2 authors at 1 institution in 1 country.
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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.
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