Evidence map›Paper›PMID 29932054›Full record

ReviewJournal of genetics2018

Transcriptional modulation of entire chromosomes: dosage compensation.

John C Lucchesi

Abstract readReview
PubMed
In one paragraph

Review in Journal of genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. N-terminus ofeLife · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. A Connectomic Hypothesis for the Hominization of the Brain.Cerebral cortex (New York, N.Y. : 1991) · 2021
    Article
  9. Dosage compensation inJournal of genetics · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. eLife · 2019
    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

1 author at 1 institution in 1 country.

John C LucchesiDepartment of Biology, Emory University, Atlanta, GA 30322, USA. E-mail: jclucch@emory.edu.
Emory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dosage compensation is a regulatory system designed to equalize the transcription output of the genes of the sex chromosomes that are present in different doses in the sexes (X or Z chromosome, depending on the animal species involved). Different mechanisms of dosage compensation have evolved in different animal groups. In Drosophila males, a complex (male-specific lethal) associates with the X chromosome and enhances the activity of most X-linked genes by increasing the rate of RNAPII elongation. In Caenorhabditis, a complex (dosage compensation complex) that contains a number of proteins involved in condensing chromosomes decreases the level of transcription of both X chromosomes in the XX hermaphrodite. In mammals, dosage compensation is achieved by the inactivation, early during development, of most X-linked genes on one of the two X chromosomes in females. The mechanism involves the synthesis of an RNA (Tsix) that protects one of the two Xs from inactivation, and of another RNA (Xist) that coats the other X chromosome and recruits histone and DNA modifying enzymes. This review will focus on the current progress in understanding the dosage compensation mechanisms in the three taxa where it has been best studied at the molecular level: flies, round worms and mammals.

Indexed as

Dosage Compensation, GeneticTranscription, GeneticAnimalsCaenorhabditis elegansDrosophila melanogasterFemaleGenes, X-LinkedMaleX Chromosome

Identifiers

PMID29932054
OpenAlexW2801758006

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.