Evidence map›Paper›PMID 29069448›Full record

ArticleNucleic acids research2017

Asymmetric cell division requires specific mechanisms for adjusting global transcription.

Adriana Mena, Daniel A Medina, José García-Martínez, Victoria Begley, Abhyudai Singh, Sebastián Chávez, Mari C Muñoz-Centeno, José E Pérez-Ortín

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  5. Article
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  7. Article
  8. Eukaryotic RNA Polymerases: The Many Ways to Transcribe a Gene.Frontiers in molecular biosciences · 2021
    Review
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  10. Article
  11. 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 3 institutions in 2 countries.

Adriana MenaDepartamento de Bioquímica y Biología Molecular and E.R.I. Biotecmed, Universitat de València, Dr. Moliner, 50, Burjassot 46100, Valencia, Spain.
Daniel A MedinaDepartamento de Bioquímica y Biología Molecular and E.R.I. Biotecmed, Universitat de València, Dr. Moliner, 50, Burjassot 46100, Valencia, Spain.
José García-MartínezDepartamento de Genética and E.R.I. Biotecmed, Universitat de València, Dr. Moliner, 50, Burjassot 46100, Valencia, Spain.
Victoria BegleyDepartamento de Genética, Universidad de Sevilla and Instituto de Biomedicina de Sevilla (IBiS), Hospital Virgen del Rocío-CSIC-Universidad de Sevilla, 41013 Sevilla, Spain.
Abhyudai SinghDepartment of Electrical and Computer Engineering, University of Delaware, Newark, DE 19716, USA.
Sebastián ChávezDepartamento de Genética, Universidad de Sevilla and Instituto de Biomedicina de Sevilla (IBiS), Hospital Virgen del Rocío-CSIC-Universidad de Sevilla, 41013 Sevilla, Spain.
Mari C Muñoz-CentenoDepartamento de Genética, Universidad de Sevilla and Instituto de Biomedicina de Sevilla (IBiS), Hospital Virgen del Rocío-CSIC-Universidad de Sevilla, 41013 Sevilla, Spain.
José E Pérez-OrtínDepartamento de Bioquímica y Biología Molecular and E.R.I. Biotecmed, Universitat de València, Dr. Moliner, 50, Burjassot 46100, Valencia, Spain.
Universitat de València · ESInstituto de Biomedicina de Sevilla · ESUniversity of Delaware · US

Funding

Stochastic hybrid systems approach to uncovering cell-size control mechanisms R01GM126557 · NIGMS · UNIVERSITY OF DELAWARE · PI SINGH, ABHYUDAI · 2017 to 2019
$675k
NIGMS NIH HHS R01 GM126557
6 · The paper itself

Abstract

Most cells divide symmetrically into two approximately identical cells. There are many examples, however, of asymmetric cell division that can generate sibling cell size differences. Whereas physical asymmetric division mechanisms and cell fate consequences have been investigated, the specific problem caused by asymmetric division at the transcription level has not yet been addressed. In symmetrically dividing cells the nascent transcription rate increases in parallel to cell volume to compensate it by keeping the actual mRNA synthesis rate constant. This cannot apply to the yeast Saccharomyces cerevisiae, where this mechanism would provoke a never-ending increasing mRNA synthesis rate in smaller daughter cells. We show here that, contrarily to other eukaryotes with symmetric division, budding yeast keeps the nascent transcription rates of its RNA polymerases constant and increases mRNA stability. This control on RNA pol II-dependent transcription rate is obtained by controlling the cellular concentration of this enzyme.

Indexed as

RNA StabilityTranscription, GeneticCell CycleCell DivisionCell SizeDNA-Directed RNA PolymerasesRNA, MessengerRNA Polymerase ISaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA-Directed RNA PolymerasesRNA, MessengerRNA Polymerase ISaccharomyces cerevisiae Proteins

Identifiers

PMID29069448
PMCPMC5716168
OpenAlexW2766368962

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.