ArticleGenetics2002
Genetic interaction between integrins and moleskin, a gene encoding a Drosophila homolog of importin-7.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanical control of nuclear import by Importin-7 is regulated by its dominant cargo YAP.Nature communications · 2022Article
- Importin-9 regulates chromosome segregation and packaging in Drosophila germ cells.Journal of cell science · 2021Article
- Drosophila importin-7 functions upstream of the Elmo signaling module to mediate the formation and stability of muscle attachments.Journal of cell science · 2013Article
- Identification and characterization of Drosophila Snurportin reveals a role for the import receptor Moleskin/importin-7 in snRNP biogenesis.Molecular biology of the cell · 2013Article
- Interaction between IGF-IR and ER induced by E2 and IGF-I.PloS one · 2013Article
- Moleskin is essential for the formation of the myotendinous junction in Drosophila.Developmental biology · 2011Article
- Preferential utilization of Imp7/8 in nuclear import of Smads.The Journal of biological chemistry · 2008Article
- Nuclear localization of the ERK MAP kinase mediated by Drosophila alphaPS2betaPS integrin and importin-7.Molecular biology of the cell · 2007Article
- Msk is required for nuclear import of TGF-{beta}/BMP-activated Smads.The Journal of cell biology · 2007Article
- Delta and Egfr expression are regulated by Importin-7/Moleskin in Drosophila wing development.Developmental biology · 2007Article
- A genetic screen in Drosophila for genes interacting with senseless during neuronal development identifies the importin moleskin.Genetics · 2007Article
- smoothened and thickveins regulate Moleskin/Importin 7-mediated MAP kinase signaling in the developing Drosophila eye.Development (Cambridge, England) · 2006Article
- MAP kinase subcellular localization controls both pattern and proliferation in the developing Drosophila wing.Development (Cambridge, England) · 2006Article
- Identification of integrin beta subunit mutations that alter heterodimer function in situ.Molecular biology of the cell · 2004Article
- Transcriptional signature of an adult brain tumor in Drosophila.BMC genomics · 2004Article
- "Importin" signaling roles for import proteins: the function of Drosophila importin-7 (DIM-7) in muscle-tendon signaling.Cell adhesion & migrationArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The Drosophila PS1 and PS2 integrins are required to maintain the connection between the dorsal and ventral wing epithelia. If alphaPS subunits are inappropriately expressed during early pupariation, the epithelia separate, causing a wing blister. Two lines of evidence indicate that this apparent loss-of-function phenotype is not a dominant negative effect, but is due to inappropriate expression of functional integrins: wing blisters are not generated efficiently by misexpression of loss-of-function alphaPS2 subunits with mutations that inhibit ligand binding, and gain-of-function, hyperactivated mutant alphaPS2 proteins cause blistering at expression levels well below those required by wild-type proteins. A genetic screen for dominant suppressors of wing blisters generated null alleles of a gene named moleskin, which encodes the protein DIM-7. DIM-7, a Drosophila homolog of vertebrate importin-7, has recently been shown to bind the SHP-2 tyrosine phosphatase homolog Corkscrew and to be important in the nuclear translocation of activated D-ERK. Consistent with this latter finding, homozygous mutant clones of moleskin fail to grow in the wing. Genetic tests suggest that the moleskin suppression of wing blisters is not directly related to inhibition of D-ERK nuclear import. These data are discussed with respect to the possible regulation of integrin function by cytoplasmic ERK.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.