Evidence map›Paper›PMID 23052823›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2012

Milk ejection in mice LG/J x SM/J.

Carolina P Góes, Bruno Sauce, Andrea C Peripato

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Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 88% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 2 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Carolina P GóesDepartment of Genetics and Evolution, Biological Science and Health Center, Federal University of Sao Carlos, Via Washington Luiz Km 235, Sao Carlos, SP, 13565-905, Brazil.
Bruno Sauce
Andrea C Peripato
Universidade Federal de São Carlos · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mammals, milk provision is crucial to offspring survival and growth from birth to weaning. Milk deficiency early in life may cause death or changes in the progeny metabolism that later may lead to obesity and metabolic disorders. This study investigates milk ejection (ME) the first day after birth (D1) in F(2) females from the intercross of LG/J and SM/J inbred mice strains. The absence of milk in F(3) pups' stomach at D1 is directly associated with their survival (p < 0.001) and growth pattern (p < 0.001) in the early stages of life. Furthermore, late growth pattern is also affected by this lack of nutrients at D1 because pups that survive this absence, mostly males, are heavier at weaning (p < 0.001) which, after necropsy, is shown to be due to significant higher total fat deposition (p < 0.01). We performed QTL analysis for ME at D1 in these F(2) females. Maternal performance of ME revealed a complex genetic architecture which even though it contains only a single QTL (accounting for 8 % of the variation in ME), it is totally context-dependent on the genetic background. We discovered many regions involved in epistatic interactions that together with the single QTL explain 19 % of the genetic variation for this trait. Milk ejection is an important component of maternal care, and understanding the mechanisms modulating its variation, along with other maternal features, may help to disentangle the complexity that is the mother/offspring relationship.

Indexed as

Genetic VariationAnimalsBody WeightCrosses, GeneticEpistasis, GeneticFemaleGenotypeMaleMiceMice, Inbred StrainsMilk EjectionQuantitative Trait LociWeaning

Identifiers

PMID23052823
OpenAlexW2075442752

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.