ArticlePLoS genetics2013
Histone variant HTZ1 shows extensive epistasis with, but does not increase robustness to, new mutations.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Gim3 buffers and potentiates de novo mutations that affect fluconazole susceptibility in yeast.EMBO reports · 2026Article
- The Hsp90 Molecular Chaperone as a Global Modifier of the Genotype-Phenotype-Fitness Map: An Evolutionary Perspective.Journal of molecular biology · 2024Review
- Selection for robust metabolism in domesticated yeasts is driven by adaptation to Hsp90 stress.Science (New York, N.Y.) · 2024Article
- Spontaneous single-nucleotide substitutions and microsatellite mutations have distinct distributions of fitness effects.PLoS biology · 2024Article
- Mutational robustness and the role of buffer genes in evolvability.The EMBO journal · 2024Review
- The limitations of phenotype prediction in metabolism.PLoS computational biology · 2023Article
- The Architecture of Metabolic Networks Constrains the Evolution of Microbial Resource Hierarchies.Molecular biology and evolution · 2023Article
- Developmental phenomics suggests that H3K4 monomethylation confers multi-level phenotypic robustness.Cell reports · 2022Article
- Genotype by environment interaction for gene expression in Drosophila melanogaster.Nature communications · 2020Article
- Genetic buffering and potentiation in metabolism.PLoS computational biology · 2020Article
- Extent and context dependence of pleiotropy revealed by high-throughput single-cell phenotyping.PLoS biology · 2020Article
- EvoChromo: towards a synthesis of chromatin biology and evolution.Development (Cambridge, England) · 2019Review
- The developmental-genetics of canalization.Seminars in cell & developmental biology · 2019Review
- Decanalizing thinking on genetic canalization.Seminars in cell & developmental biology · 2019Review
- Analysis of Epistasis in Natural Traits Using Model Organisms.Trends in genetics : TIG · 2018Review
- Chaperones, Canalization, and Evolution of Animal Forms.International journal of molecular sciences · 2018Review
- The complex underpinnings of genetic background effects.Nature communications · 2018Article
- A sibling method for identifying vQTLs.PloS one · 2018Article
- Modifiers of the Genotype-Phenotype Map: Hsp90 and Beyond.PLoS biology · 2016Review
- Article
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5 authors.
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Abstract
Biological systems produce phenotypes that appear to be robust to perturbation by mutations and environmental variation. Prior studies identified genes that, when impaired, reveal previously cryptic genetic variation. This result is typically interpreted as evidence that the disrupted gene normally increases robustness to mutations, as such robustness would allow cryptic variants to accumulate. However, revelation of cryptic genetic variation is not necessarily evidence that a mutationally robust state has been made less robust. Demonstrating a difference in robustness requires comparing the ability of each state (with the gene perturbed or intact) to suppress the effects of new mutations. Previous studies used strains in which the existing genetic variation had been filtered by selection. Here, we use mutation accumulation (MA) lines that have experienced minimal selection, to test the ability of histone H2A.Z (HTZ1) to increase robustness to mutations in the yeast Saccharomyces cerevisiae. HTZ1, a regulator of chromatin structure and gene expression, represents a class of genes implicated in mutational robustness. It had previously been shown to increase robustness of yeast cell morphology to fluctuations in the external or internal microenvironment. We measured morphological variation within and among 79 MA lines with and without HTZ1. Analysis of within-line variation confirms that HTZ1 increases microenvironmental robustness. Analysis of between-line variation shows the morphological effects of eliminating HTZ1 to be highly dependent on the line, which implies that HTZ1 interacts with mutations that have accumulated in the lines. However, lines without HTZ1 are, as a group, not more phenotypically diverse than lines with HTZ1 present. The presence of HTZ1, therefore, does not confer greater robustness to mutations than its absence. Our results provide experimental evidence that revelation of cryptic genetic variation cannot be assumed to be caused by loss of robustness, and therefore force reevaluation of prior claims based on that assumption.
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