ArticleGenes & development2007
Modeling complex genetic interactions in a simple eukaryotic genome: actin displays a rich spectrum of complex haploinsufficiencies.
Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
53 citing papers in PubMed, 86 citations in OpenAlex.
- Ribosomal protein paralogues in ribosome specialization.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Loss of cytoplasmic actin filaments raises nuclear actin levels to drive INO80C-dependent chromosome fragmentation.Nature communications · 2024Article
- Purification of human β- and γ-actin from budding yeast.Journal of cell science · 2023Article
- From systems to structure - using genetic data to model protein structures.Nature reviews. Genetics · 2022Review
- Cytoduction and Plasmiduction in Yeast.Bio-protocol · 2021Article
- Article
- A novel genetic circuitry governing hypoxic metabolic flexibility, commensalism and virulence in the fungal pathogen Candida albicans.PLoS pathogens · 2019Article
- Does functional specialization of ribosomes really exist?RNA (New York, N.Y.) · 2019Review
- Systematic Complex Haploinsufficiency-Based Genetic Analysis ofG3 (Bethesda, Md.) · 2018Article
- Specialized ribosomes and specific ribosomal protein paralogs control translation of mitochondrial proteins.The Journal of cell biology · 2018Article
- Mapping a diversity of genetic interactions in yeast.Current opinion in systems biology · 2017Article
- Genetic analysis of the Candida albicans biofilm transcription factor network using simple and complex haploinsufficiency.PLoS genetics · 2017Article
- Paralog-Specific Functions ofG3 (Bethesda, Md.) · 2017Article
- Article
- Mutant power: using mutant allele collections for yeast functional genomics.Briefings in functional genomics · 2016Review
- The Modular Adaptive Ribosome.PloS one · 2016Article
- Genome-wide synthetic genetic screening by transposon mutagenesis in Candida albicans.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Site-specific cation release drives actin filament severing by vertebrate cofilin.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Linking genetics to structural biology: complex heterozygosity screening with actin alanine scan alleles identifies functionally related surfaces on yeast actin.G3 (Bethesda, Md.) · 2014Article
- Mechanisms of nuclear actin in chromatin-remodeling complexes.Trends in cell biology · 2014Review
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5 authors at 2 institutions in 1 country.
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Abstract
Multigenic influences are major contributors to human genetic disorders. Since humans are highly polymorphic, there are a high number of possible detrimental, multiallelic gene pairs. The actin cytoskeleton of yeast was used to determine the potential for deleterious bigenic interactions; approximately 4800 complex hemizygote strains were constructed between an actin-null allele and the nonessential gene deletion collection. We found 208 genes that have deleterious complex haploinsufficient (CHI) interactions with actin. This set is enriched for genes with gene ontology terms shared with actin, including several actin-binding protein genes, and nearly half of the CHI genes have defects in actin organization when deleted. Interactions were frequently seen with genes for multiple components of a complex or with genes involved in the same function. For example, many of the genes for the large ribosomal subunit (RPLs) were CHI with act1Delta and had actin organization defects when deleted. This was generally true of only one RPL paralog of apparently duplicate genes, suggesting functional specialization between ribosomal genes. In many cases, CHI interactions could be attributed to localized defects on the actin protein. Spatial congruence in these data suggest that the loss of binding to specific actin-binding proteins causes subsets of CHI interactions.
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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.