Evidence map›Paper›PMID 27485376›Full record

ReviewNucleus (Austin, Tex.)2016

A role for Rtt109 in buffering gene-dosage imbalance during DNA replication.

Yoav Voichek, Raz Bar-Ziv, Naama Barkai

Abstract readReview
In one paragraph

Review in Nucleus (Austin, Tex.), 2016. 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
–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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. 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

3 authors.

Yoav Voicheka Department of Molecular Genetics , Weizmann Institute of Science , Rehovot , Israel.
Raz Bar-Ziva Department of Molecular Genetics , Weizmann Institute of Science , Rehovot , Israel.
Naama Barkaia Department of Molecular Genetics , Weizmann Institute of Science , Rehovot , Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromatin can function as an integrator of DNA-related processes, allowing communication, for example, between DNA replication and gene transcription. Such communication is needed to overcome the gene-dosage imbalance introduced during DNA replication, when certain genes are replicated prior to others. Increased transcription of early replicating genes could alter regulatory balances. This does not occur, suggesting a mechanism that suppresses expression from newly replicated DNA. Critical to this buffering is Rtt109, which acetylates the internal K56 residue of newly synthesized histone H3 prior to incorporation onto DNA. H3K56ac distinguishes replicated from non-replicated DNA, communicating this information to the transcription machinery to ensure expression homeostasis during S phase.

Indexed as

Gene DosageChromatinDNA ReplicationGene Expression RegulationHistone AcetyltransferasesHomeostasisHumansChromatinHistone AcetyltransferasesChromatinDNA replicationgene expressionH3K56acRTT109

Identifiers

PMID27485376
PMCPMC5038999

What OpenQuestion holds

Textmetadata
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.