Evidence map›Paper›PMID 20813847›Full record

ArticleThe Journal of biological chemistry2010

Proliferating cell nuclear antigen (PCNA) is required for cell cycle-regulated silent chromatin on replicated and nonreplicated genes.

Andrew Miller, Jiji Chen, Taichi E Takasuka, Jennifer L Jacobi, Paul D Kaufman, Joseph M K Irudayaraj, Ann L Kirchmaier

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Additions toMycoKeys · 2023
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  3. The Use of Yeast in Biosensing.Microorganisms · 2022
    Review
  4. Article
  5. Article
  6. FRET Microscopy in Yeast.Biosensors · 2019
    Review
  7. Article
  8. Article
  9. Proliferating cell nuclear antigen (PCNA) contributes to the high-order structure and stability of heterochromatin in Saccharomyces cerevisiae.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2017
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Inside single cells: quantitative analysis with advanced optics and nanomaterials.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology
    Review
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

7 authors at 3 institutions in 1 country.

Andrew MillerDepartment of Biochemistry, Purdue University Center for Cancer Research, Purdue University, West Lafayette, Indiana 47907, USA.
Jiji Chen
Taichi E Takasuka
Jennifer L Jacobi
Paul D Kaufman
Joseph M K Irudayaraj
Ann L Kirchmaier
Purdue University West Lafayette · USCenter for Cancer Research · USUniversity of Massachusetts Chan Medical School · US

Funding

GENETIC ANALYSIS OF THE GENES CONTROLLING A POSITIONR01GM031105 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI RINE, JASPER D · 1985 to 2020
$6.4M
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
GENETIC ANALYSIS OF GENES CONTROLLING A POSITION EFFECTR37GM031105 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI RINE, JASPER D · 1999 to 2008
$3.5M
NIGMS NIH HHS GM31105NIGMS NIH HHS R01 GM031105NIGMS NIH HHS R01 GM055712NIGMS NIH HHS R01 GM55712NIGMS NIH HHS R37 GM031105
6 · The paper itself

Abstract

In Saccharomyces cerevisiae, silent chromatin is formed at HMR upon the passage through S phase, yet neither the initiation of DNA replication at silencers nor the passage of a replication fork through HMR is required for silencing. Paradoxically, mutations in the DNA replication processivity factor, POL30, disrupt silencing despite this lack of requirement for DNA replication in the establishment of silencing. We tested whether pol30 mutants could establish silencing at either replicated or non-replicated HMR loci during S phase and found that pol30 mutants were defective in establishing silencing at HMR regardless of its replication status. Although previous studies tie the silencing defect of pol30 mutants to the chromatin assembly factors Asf1p and CAF-1, we found pol30 mutants did not exhibit a gross defect in packaging HMR into chromatin. Rather, the pol30 mutants exhibited defects in histone modifications linked to ASF1 and CAF-1-dependent pathways, including SAS-I- and Rtt109p-dependent acetylation events at H4-K16 and H3-K9 (plus H3-K56; Miller, A., Yang, B., Foster, T., and Kirchmaier, A. L. (2008) Genetics 179, 793-809). Additional experiments using FLIM-FRET revealed that Pol30p interacted with SAS-I and Rtt109p in the nuclei of living cells. However, these interactions were disrupted in pol30 mutants with defects linked to ASF1- and CAF-1-dependent pathways. Together, these results imply that Pol30p affects epigenetic processes by influencing the composition of chromosomal histone modifications.

Indexed as

AcetylationAntigens, NuclearCell Cycle ProteinsChromatinChromosomes, FungalDNA, FungalDNA ReplicationGene SilencingGenetic LociHistone AcetyltransferasesHistonesMolecular ChaperonesMutationProliferating Cell Nuclear AntigenRibonucleasesSaccharomyces cerevisiaeAntigens, NuclearASF1 protein, S cerevisiaeCell Cycle ProteinsChromatinDNA, FungalHistone AcetyltransferasesHistonesMolecular ChaperonesPOL30 protein, S cerevisiaePOP2 protein, S cerevisiaeProliferating Cell Nuclear AntigenRibonucleasesRtt109 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID20813847
PMCPMC2966128
OpenAlexW2004407614

What OpenQuestion holds

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Registered trials

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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.