Evidence map›Paper›PMID 23666922›Full record

ArticleGenes & development2013

Molecular antagonism between X-chromosome and autosome signals determines nematode sex.

Behnom Farboud, Paola Nix, Margaret M Jow, John M Gladden, Barbara J Meyer

Abstract read
In one paragraph

Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
  2. Aberrant X chromosome dosage compensation causes hybrid male inviability inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Sex matters in preclinical research.Disease models & mechanisms · 2024
    Article
  7. Review
  8. The X chromosome in C. elegans sex determination and dosage compensation.Current opinion in genetics & development · 2022
    Review
  9. Review
  10. Sex Determination in Nematode Germ Cells.Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation · 2022
    Review
  11. DMRT1 gene disruption alone induces incomplete gonad feminization in chicken.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Sex-Specific Gene Expression and Life Span Regulation.Trends in endocrinology and metabolism: TEM · 2017
    Review
  18. Article
  19. Article
  20. Balancing up and downregulation of the C. elegans X chromosomes.Current opinion in genetics & development · 2015
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Behnom FarboudHoward Hughes Medical Institute, Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 94720, USA.
Paola Nix
Margaret M Jow
John M Gladden
Barbara J Meyer

Funding

POSTGRADUATE TRAINING PROGRAM IN GENETICST32GM007127 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI DILLIN, ANDREW G · 1985 to 2016
$7.9M
NEMATODE SEX DETERMINATIONR01GM030702 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MEYER, BARBARA J · 1985 to 2018
$6.1M
NIGMS NIH HHS R01 GM030702NIGMS NIH HHS R01-GM30702NIGMS NIH HHS T32 GM007127NIGMS NIH HHS T32-GM07127
6 · The paper itself

Abstract

Sex is determined in Caenorhabditis elegans by the ratio of X chromosomes to the sets of autosomes, the X:A signal. A set of genes called X signal elements (XSEs) communicates X-chromosome dose by repressing the masculinizing sex determination switch gene xol-1 (XO lethal) in a dose-dependent manner. xol-1 is active in 1X:2A embryos (males) but repressed in 2X:2A embryos (hermaphrodites). Here we showed that the autosome dose is communicated by a set of autosomal signal elements (ASEs) that act in a cumulative, dose-dependent manner to counter XSEs by stimulating xol-1 transcription. We identified new ASEs and explored the biochemical basis by which ASEs antagonize XSEs to determine sex. Multiple antagonistic molecular interactions carried out on a single promoter explain how different X:A values elicit different sexual fates. XSEs (nuclear receptors and homeodomain proteins) and ASEs (T-box and zinc finger proteins) bind directly to several sites on xol-1 to counteract each other's activities and thereby regulate xol-1 transcription. Disrupting ASE- and XSE-binding sites in vivo recapitulated the misregulation of xol-1 transcription caused by disrupting cognate signal element genes. XSE- and ASE-binding sites are distinct and nonoverlapping, suggesting that direct competition for xol-1 binding is not how XSEs counter ASEs. Instead, XSEs likely antagonize ASEs by recruiting cofactors with reciprocal activities that induce opposite transcriptional states. Most ASE- and XSE-binding sites overlap xol-1's -1 nucleosome, which carries activating chromatin marks only when xol-1 is turned on. Coactivators and corepressors tethered by proteins similar to ASEs and XSEs are known to deposit and remove such marks. The concept of a sex signal comprising competing XSEs and ASEs arose as a theory for fruit flies a century ago. Ironically, while the recent work of others showed that the fly sex signal does not fit this simple paradigm, our work shows that the worm signal does.

Indexed as

Amino Acid MotifsAnimalsAsparagineBinding SitesCaenorhabditis elegansCaenorhabditis elegans ProteinsCell NucleusChromosomesDNA-Binding ProteinsDNA Transposable ElementsDosage Compensation, GeneticEmbryo, NonmammalianFemaleGene DosageGene Expression Regulation, DevelopmentalGenes, HelminthAsparagineCaenorhabditis elegans ProteinsCEH-39 protein, C elegansDNA-Binding ProteinsDNA Transposable ElementsGlutamineHomeodomain Proteinsmariner transposasesReceptors, Cytoplasmic and NuclearRNA-Binding ProteinsSEA-2 protein, C eleganssex-1 protein, C elegansTransposasesXOL-1 protein, C elegansdosage compensationdose-sensitive signalshaploinsufficiencynuclear hormone receptorsex determinationT-box protein

Identifiers

PMID23666922
PMCPMC3672649

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.