Evidence map›Paper›PMID 16245026›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2005

Genetic and parent-of-origin influences on X chromosome choice in Xce heterozygous mice.

Lisa Helbling Chadwick, Huntington F Willard

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Frontiers in cell and developmental biology · 2022
    Article
  3. Article
  4. Review
  5. The Role of X-Chromosome Inactivation in Retinal Development and Disease.Advances in experimental medicine and biology · 2016
    Article
  6. Sex-Specific Parental Effects on Offspring Lipid Levels.Journal of the American Heart Association · 2015
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. X-inactivation analysis of embryonic lethality in Ocrl wt/-; Inpp5b-/- mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2010
    Article
  13. Article
  14. Article
  15. Article
  16. 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.

Lisa Helbling ChadwickInstitute for Genome Sciences & Policy, Duke University, Durham, North Carolina 27708, USA.
Huntington F Willard

Funding

MOLECULAR GENETICS OF HUMAN X CHROMOSOME INACTIVATIONR01GM045441 · NIGMS · STANFORD UNIVERSITY · PI WILLARD, HUNTINGTON F · 1991 to 1999
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NIGMS NIH HHS GM45441
6 · The paper itself

Abstract

X chromosome inactivation is unique among dosage compensation mechanisms in that the two X chromosomes in females are treated differently within the same cell; one X chromosome is stably silenced while the other remains active. It is widely believed that, when X inactivation is initiated, each cell makes a random choice of which X chromosome will be silenced. In mice, only one genetic locus, the X-linked X controlling element (X ce), is known to influence this choice, because animals that are heterozygous at X ce have X-inactivation patterns that differ markedly from a mean of 0.50. To document other genetic and epigenetic influences on choice, we have performed a population-based study of the effect of X ce genotype on X-inactivation patterns. In B 6 CAST F(1) females (X ce(b)/X ce(c)), the X-inactivation pattern followed a symmetric distribution with a mean of 0.29 (SD=0.08). Surprisingly, however, in a population of X ce(b)/X ce(c) heterozygous B 6 CAST F(2) females, we observed significant differences in both the mean (p=0.004) and variance (p=0.004) of the X-inactivation patterns. This finding is incompatible with a single-locus model and suggests that additional genetic factors also influence X chromosome choice. We show that both parent-of-origin and naturally occurring genetic variation at autosomal loci contribute to these differences. Taken together, these data reveal further genetic complexity in this epigenetic control pathway.

Indexed as

Genetic VariationModels, GeneticAnimalsCrosses, GeneticCyclin-Dependent KinasesDNA PrimersGenes, X-LinkedGenotypeInheritance PatternsMiceMicrosatellite RepeatsProtein Serine-Threonine KinasesX Chromosome InactivationCyclin-Dependent KinasesDNA PrimersPCTAIRE-1 protein kinaseProtein Serine-Threonine Kinases

Identifiers

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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.