Evidence map›Paper›PMID 35986361›Full record

ArticleEpigenetics & chromatin2022

An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae.

Rachel M Reardon, Amanda K Walsh, Clairine I Larsen, LauraAnn H Schmidberger, Lillian A Morrow, Adriane E Thompson, Isabel M Wellik, Jeffrey S Thompson

Open access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 31% of its field
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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Zeocin-Induced Adaptive Response inMolecules (Basel, Switzerland) · 2026
    Article
  2. The Growth, Pathogenesis, and Secondary Metabolism ofJournal of fungi (Basel, Switzerland) · 2025
    Article
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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

8 authors at 6 institutions in 1 country.

Rachel M ReardonDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA.
Amanda K WalshDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA.
Clairine I LarsenDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA.
LauraAnn H SchmidbergerDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA.
Lillian A MorrowDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA.
Adriane E ThompsonDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA.
Isabel M WellikDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA.
Jeffrey S ThompsonDepartment of Biology, Denison University, 213 Talbot Hall, 100 W. College St., Granville, OH, 43023, USA. thompsonjs@denison.edu.ORCID 0000-0002-9281-2596
Denison University · USGrinnell College · USHarvard University · USScripps Research Institute · USUniversity of California, San Francisco · USUniversity of Wisconsin–Madison · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpigenetics refers to inheritable phenotypic changes that occur in the absence of genetic alteration. Such adaptations can provide phenotypic plasticity in reaction to environmental cues. While prior studies suggest that epigenetics plays a role in the response to DNA damage, no direct demonstration of epigenetically inheritable processes have been described in this context.

resultsHere we report the identification of an epigenetic response to ultraviolet (UV) radiation in the baker's yeast Saccharomyces cerevisiae. Cells that have been previously exposed to a low dosage of UV exhibit dramatically increased survival following subsequent UV exposure, which we refer to as UV hyper-resistance (UVHR). This phenotypic change persists for multiple mitotic generations, without any indication of an underlying genetic basis. Pre-exposed cells experience a notable reduction in the amount of DNA damage caused by the secondary UV exposure. While the mechanism for the protection is not fully characterized, our results suggest that UV-induced cell size increases and/or cell wall changes are contributing factors. In addition, we have identified two histone modifications, H3K56 acetylation and H3K4 methylation, that are important for UVHR, potentially serving as mediators of UV protective gene expression patterns, as well as epigenetic marks to propagate the phenotype across cell generations.

conclusionsExposure to UV radiation triggers an epigenetically inheritable protective response in baker's yeast that increases the likelihood of survival in response to subsequent UV exposures. These studies provide the first demonstration of an epigenetically inheritable dimension of the cellular response to DNA damage.

Indexed as

Saccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA DamageHistonesPhenotypeHistonesSaccharomyces cerevisiae ProteinsCell sizeCell wallDNA damageEpigeneticsHistone acetylationHistone methylationUVYeast

Identifiers

PMID35986361
PMCPMC9392361
OpenAlexW4292395126

What OpenQuestion holds

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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.