Evidence map›Paper›PMID 19796999›Full record

ArticleDNA repair2009

A negatively charged residue in place of histone H3K56 supports chromatin assembly factor association but not genotoxic stress resistance.

Judith A Erkmann, Paul D Kaufman

Abstract read
In one paragraph

Article in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Cell cycle-dependent changes in H3K56ac in human cells.Cell cycle (Georgetown, Tex.) · 2015
    Article
  6. Article
  7. A small molecule inhibitor of fungal histone acetyltransferase Rtt109.Bioorganic & medicinal chemistry letters · 2013
    Article
  8. Article
  9. Chromatin-mediated Candida albicans virulence.Biochimica et biophysica acta · 2012
    Article
  10. Article
  11. Article
  12. Catalytic activation of histone acetyltransferase Rtt109 by a histone chaperone.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  13. Article
  14. Histone acetyltransferase Rtt109 is required for Candida albicans pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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

2 authors at 1 institution in 1 country.

Judith A ErkmannProgram in Gene Function and Expression, University of Massachusetts Medical School, 364 Plantation St. #506, Worcester, MA 01605, USA.
Paul D Kaufman
University of Massachusetts Chan Medical School · US

Funding

Regulation of repetitive chromatin structures during the human cell cycleR01GM055712 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KAUFMAN, PAUL D. · 1997 to 2014
$5.1M
Roles of PCNA and Asf1 in the Replication CheckpointF32GM075601 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ERKMANN, JUDITH A · 2005 to 2007
$151k
NIGMS NIH HHS 1 F32 GM075601-01NIGMS NIH HHS F32 GM075601NIGMS NIH HHS R01 GM055712NIGMS NIH HHS R01 GM55712
6 · The paper itself

Abstract

In fungal species, lysine 56 of newly synthesized histone H3 molecules is modified by the acetyltransferase Rtt109, which promotes resistance to genotoxic agents. To further explore how H3 K56ac contributes to genome stability, we conducted screens for suppressors of the DNA damage sensitivity of budding yeast rtt109 Delta mutants. We recovered a single extragenic suppressor mutation that efficiently restored damage resistance. The suppressor is a point mutation in the histone H3 gene HHT2, and converts lysine 56 to glutamic acid. In some ways, K56E mimics K56ac, because it suppresses other mutations that interfere with the production of H3 K56ac and restores histone binding to chromatin assembly proteins CAF-1 and Rtt106. Therefore, we demonstrate that enhanced association with chromatin assembly factors can be accomplished not only by acetylation-mediated charge neutralization of H3K56 but also by the replacement of the positively charged lysine with an acidic residue. These data suggest that removal of the positive charge on lysine 56 is the functionally important consequence of H3K56 acetylation. Additionally, the suppressive function of K56E requires the presence of a second H3 allele, because K56E impairs growth when it is the sole source of histones, even more so than does constitutive H3K56 acetylation. Our studies therefore emphasize how H3 K56ac not only promotes chromatin assembly but also leads to chromosomal malfunction if not removed following histone deposition.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, FungalAllelesDNA DamageHistone AcetyltransferasesHistonesMutationPhenotypeSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsHistone AcetyltransferasesHistonesRtt109 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID19796999
PMCPMC2787813
OpenAlexW1991253230

What OpenQuestion holds

Textmetadata
LicenceTDM
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.