Effect of SOCS2 R96C mutation on mouse mammary gland development and function
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ABSTRACT:
PROVIDER: PRJNA935704 | ENA |
REPOSITORIES: ENA
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Project description:The R96C mutation in SOCS2 (suppressor of cytokine signaling 2) that leads to greater milk production but also a greater sensitivity to mastitis was identified in Lacaune sheep by Rupp et al, 2015. This mutation leads to a loss of ligand recognition for SOCS2 and thus interferes with JAK/STAT signaling pathway regulation. A mouse model carrying this mutation (SOCS2 R96C KI) was developed to study its effects on mammary gland development and lactation.
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Project description:This submission contains the mass spectrometry files for the manuscript by Aurelie Lacouture et al. that describes the quantitative proteomics analysis of mouse mammary gland epithelial organoids proteome. Experiments were performed from mammary glands organoids derived from mouse and the MS files were acquired on Orbitrap Fusion mass spectrometer. For questions, please contact Etienne Audet-Walsh (Etienne.Audet-Walsh@crchudequebec.ulaval.ca).
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Project description:Analysis of protein tyrosine phosphatase 1B (PTP1B) deficient mammary glands from nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15. We used a genetically ablated PTP1B mouse model to gain a deeper knowledge of the role PTP1B plays in mammary gland development and to define the mechanism regulated by this phosphatase. Results provide insight into the role of PTP1B in mammary gland development and differentiation. Mouse mammary glands were isolated from PTP1B -/- and PTP1B +/+ nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15 for RNA extraction and hybridization on Affymetrix microarrays.
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Project description:SOCS2 Ensures Metabolic Function and Mass Restoration During Liver Regeneration - SOCS2 plays distinct and contrasting roles during liver regeneration. Early after injury, SOCS2 expression increases and limits the rate of regeneration, preserving metabolic activity. Surprisingly, at later times, the role of SOCS2 reverses to promote liver regeneration by stimulating GH release from the pituitary via effects on serum levels of insulin-like growth factor 1. Loss of SOCS2 promotes GH signaling by increasing growth hormone receptor levels and driving phosphorylation of proteins in the GH pathway, establishing a state of hyper-responsiveness to GH. These findings suggest a single protein can play contrasting roles at different times after liver injury and modulation of GH signaling achieves an optimal rate of liver regeneration to balance metabolic and restorative needs. To further understand the mechanism by which SOCS2 increases early liver regeneration, we performed microarray analysis of Socs2-null mice wildtype mice at 24 and 36 hours after hepatectomy. C57BL/6 mice where used as wildtype controls. Socs2-null animals were maintained on a C57BL/6 background. Both wildtype and Socs2-null adult mice were subjected to 2/3 hepatectomy and liver tissue isolated at 24 hours and 36 hours post hepatectomy. Time zero was without hepatectomy in age-matched mice for each genotype. Total RNA isolated from collected liver tissues was pooled for three animals at each time point and two biological replicates (3 pooled liver RNAs each) were labeled for array analysis. This results in a total of 12 microarrays.
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