Evidence map›Paper›PMID 22215617›Full record

ArticleMolecular and cellular biology2012

New mutations at the imprinted Gnas cluster show gene dosage effects of Gsα in postnatal growth and implicate XLαs in bone and fat metabolism but not in suckling.

Sally A Eaton, Christine M Williamson, Simon T Ball, Colin V Beechey, Lee Moir, Jessica Edwards, Lydia Teboul, Mark Maconochie, Jo Peters

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2012. 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
3.7field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Frontiers in endocrinology · 2023
    Review
  2. Article
  3. Article
  4. Review
  5. Antisense Activity across theNon-coding RNA · 2015
    Article
  6. Article
  7. GNAS Spectrum of Disorders.Current osteoporosis reports · 2015
    Review
  8. Loss of methylation at GNAS exon A/B is associated with increased intrauterine growth.The Journal of clinical endocrinology and metabolism · 2015
    Article
  9. Article
  10. Review
  11. Postnatal establishment of allelic Gαs silencing as a plausible explanation for delayed onset of parathyroid hormone resistance owing to heterozygous Gαs disruption.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014
    Article
  12. Article
  13. Maternal inheritance of the Gnas cluster mutation Ex1A-T affects size, implicating NESP55 in growth.Mammalian genome : official journal of the International Mammalian Genome Society · 2013
    Article
  14. Review
  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

9 authors at 2 institutions in 1 country.

Sally A EatonMammalian Genetics Unit, MRC Harwell, Harwell Science and Innovation Campus, Oxfordshire, United Kingdom. s.eaton@victorchang.edu.au
Christine M Williamson
Simon T Ball
Colin V Beechey
Lee Moir
Jessica Edwards
Lydia Teboul
Mark Maconochie
Jo Peters
Mary Lyon Centre at MRC Harwell · GBUniversity of Sussex · GB

Funding

Medical Research Council MC_U142636336Medical Research Council MC_UP_1502/1Wellcome Trust
6 · The paper itself

Abstract

The imprinted Gnas cluster is involved in obesity, energy metabolism, feeding behavior, and viability. Relative contribution of paternally expressed proteins XLαs, XLN1, and ALEX or a double dose of maternally expressed Gsα to phenotype has not been established. In this study, we have generated two new mutants (Ex1A-T-CON and Ex1A-T) at the Gnas cluster. Paternal inheritance of Ex1A-T-CON leads to loss of imprinting of Gsα, resulting in preweaning growth retardation followed by catch-up growth. Paternal inheritance of Ex1A-T leads to loss of imprinting of Gsα and loss of expression of XLαs and XLN1. These mice have severe preweaning growth retardation and incomplete catch-up growth. They are fully viable probably because suckling is unimpaired, unlike mutants in which the expression of all the known paternally expressed Gnasxl proteins (XLαs, XLN1 and ALEX) is compromised. We suggest that loss of ALEX is most likely responsible for the suckling defects previously observed. In adults, paternal inheritance of Ex1A-T results in an increased metabolic rate and reductions in fat mass, leptin, and bone mineral density attributable to loss of XLαs. This is, to our knowledge, the first report describing a role for XLαs in bone metabolism. We propose that XLαs is involved in the regulation of bone and adipocyte metabolism.

Indexed as

AnimalsBone and BonesChromograninsEnergy MetabolismFemaleGene DosageGenetic LociGenomic ImprintingGTP-Binding Protein alpha Subunits, GsLipid MetabolismMaleMiceMice, KnockoutObesityProtein IsoformsSucking BehaviorChromograninsGnas protein, mouseGTP-Binding Protein alpha Subunits, GsProtein Isoforms

Identifiers

PMID22215617
PMCPMC3295192
OpenAlexW2041659862

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.