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The mammary glands of these virgin mice show a defect in the branching of the epithelial tissue. This phenotype is not compensated for at later stages of mammary development (gestation, then lactation). Mammary epithelial cell subpopulations were altered, with mutant mice having three times more basal cells and fewer luminal cells. The mammary gland of these mice remains functional; however, the mammary epithelial cells contain more lipid droplets and the lipid composition of the milk is altered. In addition, monitoring of mammary gland gene expression in virgin and then pregnant females identified around 3,000 differentially expressed genes. Analysis of the differentially expressed genes showed that multiple biological processes and signalling pathways linked to mitochondrial function and hence fatty acid oxidation are impacted. This suggests mitochondrial dysregulation and elevated oxidative stress in mammary glands. These results have enabled us to refine our knowledge of the role of SOCS2 and more specifically the R96C mutation on mammary gland development and milk production. 

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Fabienne.Le-Provost@inrae.fr