Evidence map›Paper›PMID 23990806›Full record

ArticlePLoS genetics2013

Histone variant HTZ1 shows extensive epistasis with, but does not increase robustness to, new mutations.

Joshua B Richardson, Locke D Uppendahl, Maria K Traficante, Sasha F Levy, Mark L Siegal

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Genetic buffering and potentiation in metabolism.PLoS computational biology · 2020
    Article
  11. Article
  12. Review
  13. The developmental-genetics of canalization.Seminars in cell & developmental biology · 2019
    Review
  14. Decanalizing thinking on genetic canalization.Seminars in cell & developmental biology · 2019
    Review
  15. Review
  16. Chaperones, Canalization, and Evolution of Animal Forms.International journal of molecular sciences · 2018
    Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Joshua B RichardsonCenter for Genomics and Systems Biology, Department of Biology, New York University, New York, New York, United States of America.
Locke D Uppendahl
Maria K Traficante
Sasha F Levy
Mark L Siegal

Funding

Sources and consequences of phenotypic variation in complex regulatory networksR01GM086673 · NIGMS · NEW YORK UNIVERSITY · PI SIEGAL, MARK L · 2010 to 2013
$929k
Identification of phenotypic capacitors of environmental and genotypic variationF32GM079909 · NIGMS · NEW YORK UNIVERSITY · PI LEVY, SASHA F · 2007 to 2009
$148k
NIGMS NIH HHS F32 GM079909NIGMS NIH HHS F32GM79909NIGMS NIH HHS R01 GM086673NIGMS NIH HHS R01GM086673
6 · The paper itself

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.

Indexed as

Transcription, GeneticAcetylationChromatinEpistasis, GeneticGenetic VariationHistone AcetyltransferasesHistonesMutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsChromatinHistone AcetyltransferasesHistonesHtz1 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID23990806
PMCPMC3749942

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.