Evidence map›Paper›PMID 17720939›Full record

ArticleGenetics2007

A ONECUT homeodomain protein communicates X chromosome dose to specify Caenorhabditis elegans sexual fate by repressing a sex switch gene.

John M Gladden, Barbara J Meyer

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. eIF4E assembly intobioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The X chromosome in C. elegans sex determination and dosage compensation.Current opinion in genetics & development · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Genetics · 2017
    Article
  14. Article
  15. Article
  16. Regulation of the X chromosomes in Caenorhabditis elegans.Cold Spring Harbor perspectives in biology · 2014
    Review
  17. Article
  18. Targeting X chromosomes for repression.Current opinion in genetics & development · 2010
    Review
  19. The worm solution: a chromosome-full of condensin helps gene expression go down.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2009
    Article
  20. A shared enhancer controls a temporal switch between promoters during Drosophila primary sex determination.Proceedings of the National Academy of Sciences of the United States of America · 2008
    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.

John M GladdenHoward Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley, California 94720-3204, USA.
Barbara J Meyer
Howard Hughes Medical Institute · US

Funding

NEMATODE SEX DETERMINATIONR01GM030702 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MEYER, BARBARA J · 1985 to 2018
$6.1M
NEMATODE SEX DETERMINATIONR37GM030702 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MEYER, BARBARA J · 1995 to 2004
$2.0M
NIGMS NIH HHS GM30702NIGMS NIH HHS R01 GM030702NIGMS NIH HHS R37 GM030702
6 · The paper itself

Abstract

Sex is determined in Caenorhabditis elegans through a dose-dependent signal that communicates the number of X chromosomes relative to the ploidy, the number of sets of autosomes. The sex switch gene xol-1 is the direct molecular target of this X:A signal and integrates both X and autosomal components to determine sexual fate. X chromosome number is relayed by X signal elements (XSEs) that act cumulatively to repress xol-1 in XX animals, thereby inducing hermaphrodite fate. Ploidy is relayed by autosomal signal elements (ASEs), which counteract the single dose of XSEs in XO animals to activate xol-1 and induce the male fate. Our goal was to identify and characterize new XSEs and further analyze known XSEs to understand the principles by which a small difference in the concentration of an intracellular signal is amplified to induce dramatically different developmental fates. We identified a new XSE, the ONECUT homeodomain protein CEH-39, and showed that it acts as a dose-dependent repressor of xol-1 transcript levels. Unexpectedly, most other XSEs also repress xol-1 predominantly, but not exclusively, at the transcript level. The twofold difference in X dose between XO and XX animals is translated into the male vs. hermaphrodite fate by the synergistic action of multiple, independent XSEs that render xol-1 active or inactive, primarily through transcriptional regulation.

Indexed as

Sex Determination ProcessesAnimalsAnimals, Genetically ModifiedBase SequenceCaenorhabditis elegansCaenorhabditis elegans ProteinsChromosome MappingDNA, HelminthDNA PrimersDosage Compensation, GeneticFemaleGene DosageGenes, HelminthMaleModels, BiologicalOnecut Transcription FactorsCaenorhabditis elegans ProteinsDNA, HelminthDNA PrimersOnecut Transcription FactorsXOL-1 protein, C elegans

Identifiers

PMID17720939
PMCPMC2147945
OpenAlexW2135511664

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.