Effect of SOCS2 R96C mutation on mouse mammary gland development and function

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. The gene expression in the mammary gland of homozygous wild-type and R96C SOCS2 knock-in C57BL/6 mice was analyzed in order to study the effects of the R96C SOCS2 mutation on mammary gland development and function. Mammary gland tissue with the lymph node removed at two stages of development was sequenced: virgin adult mice and mice at 18 days of gestation. Gene expression data was obtained using the Sureprint G3 Mouse gene expression v2 8*60K microarray kit.2015年吕普（Rupp）等人在拉科讷绵羊（Lacaune sheep）中鉴定到细胞因子信号转导抑制因子2（suppressor of cytokine signaling 2, SOCS2）的R96C突变，该突变可提升产奶量，但同时会增加乳腺炎易感性。该突变会导致SOCS2丧失配体识别能力，进而干扰JAK/STAT信号通路的调控功能。研究人员构建了携带该突变的小鼠模型（SOCS2 R96C敲入（knock-in, KI）小鼠），以探究其对乳腺发育与泌乳的影响。本研究对纯合野生型与R96C SOCS2敲入的C57BL/6小鼠的乳腺组织基因表达进行了分析，以明确R96C SOCS2突变对乳腺发育及功能的作用。实验选取两个发育阶段的乳腺组织（已去除淋巴结）进行测序：成年处女小鼠与妊娠18天的小鼠。基因表达数据通过Sureprint G3小鼠基因表达芯片v2 8*60K试剂盒（Sureprint G3 Mouse gene expression v2 8*60K microarray kit）获取。