ArticleGenetics2004
Drosophila crinkled, mutations of which disrupt morphogenesis and cause lethality, encodes fly myosin VIIA.
Article in Genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
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- Quantifying bristle cell organization inbioRxiv : the preprint server for biology · 2025Article
- A role for Myo-II zipper and spaghetti squash in Gliotactin-dependent Drosophila melanogaster wing hair planar cell polarity.PloS one · 2025Article
- Dusky-like Is Critical for Morphogenesis of the Cellular Protuberances and Formation of the Cuticle inBiology · 2023Article
- Unconventional Myosins fromBiomolecules · 2022Review
- Article
- Propagation of F-actin disassembly via Myosin15-Mical interactions.Science advances · 2021Article
- Spectrum ofGenes · 2021Article
- Mutations in Drosophila crinkled/Myosin VIIA disrupt denticle morphogenesis.Developmental biology · 2021Article
- A binding protein regulates myosin-7a dimerization and actin bundle assembly.Nature communications · 2021Article
- Usher Syndrome: Genetics and Molecular Links of Hearing Loss and Directions for Therapy.Frontiers in genetics · 2020Review
- Differential toxicity of ataxin-3 isoforms in Drosophila models of Spinocerebellar Ataxia Type 3.Neurobiology of disease · 2019Article
- Unanchored ubiquitin chains do not lead to marked alterations in gene expression inBiology open · 2019Article
- Expression and Regulation of Deubiquitinase-Resistant, Unanchored Ubiquitin Chains in Drosophila.Scientific reports · 2018Article
- Crumbs, Moesin and Yurt regulate junctional stability and dynamics for a proper morphogenesis of the Drosophila pupal wing epithelium.Scientific reports · 2017Article
- The unconventional myosin CRINKLED and its mammalian orthologue MYO7A regulate caspases in their signalling roles.Nature communications · 2016Article
- DnaJ-1 and karyopherin α3 suppress degeneration in a new Drosophila model of Spinocerebellar Ataxia Type 6.Human molecular genetics · 2015Article
- The Drosophila planar polarity gene multiple wing hairs directly regulates the actin cytoskeleton.Development (Cambridge, England) · 2015Article
- The diaphanous gene of Drosophila interacts antagonistically with multiple wing hairs and plays a key role in wing hair morphogenesis.PloS one · 2015Article
- Wingless/Wnt signaling in Drosophila: the pattern and the pathway.Molecular reproduction and development · 2013Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Myosin VIIs provide motor function for a wide range of eukaryotic processes. We demonstrate that mutations in crinkled (ck) disrupt the Drosophila myosin VIIA heavy chain. The ck/myoVIIA protein is present at a low level throughout fly development and at the same level in heads, thoraxes, and abdomens. Severe ck alleles, likely to be molecular nulls, die as embryos or larvae, but all allelic combinations tested thus far yield a small fraction of adult "escapers" that are weak and infertile. Scanning electron microscopy shows that escapers have defects in bristles and hairs, indicating that this motor protein plays a role in the structure of the actin cytoskeleton. We generate a homology model for the structure of the ck/myosin VIIA head that indicates myosin VIIAs, like myosin IIs, have a spectrin-like, SH3 subdomain fronting their N terminus. In addition, we establish that the two myosin VIIA FERM repeats share high sequence similarity with only the first two subdomains of the three-lobed structure that is typical of canonical FERM domains. Nevertheless, the approximately 100 and approximately 75 amino acids that follow the first two lobes of the first and second FERM domains are highly conserved among myosin VIIs, suggesting that they compose a conserved myosin tail homology 7 (MyTH7) domain that may be an integral part of the FERM domain or may function independently of it. Together, our data suggest a key role for ck/myoVIIA in the formation of cellular projections and other actin-based functions required for viability.
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