ArticleGenetics2003
Drosophila calmodulin mutants with specific defects in the musculature or in the nervous system.
Article in Genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Lipid Metabolism in Relation to Calcium Homeostasis.Advances in experimental medicine and biology · 2026Review
- Functional consequences of calmodulin variants identified among schizophrenia patients and controls.Translational psychiatry · 2025Article
- Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023Review
- Gap Junction Channelopathies and Calmodulinopathies. Do Disease-Causing Calmodulin Mutants Affect Direct Cell-Cell Communication?International journal of molecular sciences · 2021Review
- A Comparative Perspective on Functionally-Related, Intracellular Calcium Channels: The Insect Ryanodine and Inositol 1,4,5-Trisphosphate Receptors.Biomolecules · 2021Review
- Genome-wide Kdm4 histone demethylase transcriptional regulation in Drosophila.Molecular genetics and genomics : MGG · 2019Article
- Proteomic Analysis of Larval Integument in a Dominant Obese Translucent (Obs) Silkworm Mutant.Journal of insect science (Online) · 2018Article
- Comparative Analysis of the Integument Transcriptomes betweenInternational journal of molecular sciences · 2018Article
- Calmodulin mutations associated with long QT syndrome prevent inactivation of cardiac L-type Ca(2+) currents and promote proarrhythmic behavior in ventricular myocytes.Journal of molecular and cellular cardiology · 2014Article
- Divergent regulation of ryanodine receptor 2 calcium release channels by arrhythmogenic human calmodulin missense mutants.Circulation research · 2014Article
- Intracellular calcium deficits in Drosophila cholinergic neurons expressing wild type or FAD-mutant presenilin.PloS one · 2009Article
- Functional roles for beta1,4-N-acetlygalactosaminyltransferase-A in Drosophila larval neurons and muscles.Genetics · 2007Article
- Mutation of TweedleD, a member of an unconventional cuticle protein family, alters body shape in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Article
- Biochemical properties of V91G calmodulin: A calmodulin point mutation that deregulates muscle contraction in Drosophila.Protein science : a publication of the Protein Society · 2004Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have studied lethal mutations in the single calmodulin gene (Cam) of Drosophila to gain insight into the in vivo functions of this important calcium sensor. As a result of maternal calmodulin (CaM) in the mature egg, lethality is delayed until the postembryonic stages. Prior to death in the first larval instar, Cam nulls show a striking behavioral abnormality (spontaneous backward movement) whereas a mutation, Cam7, that results in a single amino acid change (V91G) produces a very different phenotype: short indented pupal cases and pupal death with head eversion defects. We show here that the null behavioral phenotype originates in the nervous system and involves a CaM function that requires calcium binding to all four sites of the protein. Further, backward movement can be induced in hypomorphic mutants by exposure to high light levels. In contrast, the V91G mutation specifically affects the musculature and causes abnormal calcium release in response to depolarization of the muscles. Genetic interaction studies suggest that failed regulation of the muscle calcium release channel, the ryanodine receptor, is the major defect underlying the Cam7 phenotype.
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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.