Project description:In this study we identifies miR-21 to by under cytokine control through the transcription factor STAT5 and while miR-21 is differentially expressed during mammary gland development, miR-21 is dispensable for mammary development and lactation.
Project description:In this study we identifies miR-21 to by under cytokine control through the transcription factor STAT5 and while miR-21 is differentially expressed during mammary gland development, miR-21 is dispensable for mammary development and lactation. We refer to wild-type mice (+/+) as WT and to mice lacking the mir-21 (-/-) as KO mice.
Project description:Cytokines control the expression of common and cell-specific genes through the transcription factor STAT5. In mammary tissue specifically, expression of approximately 570 genes is induced during pregnancy by prolactin through STAT5, which binds to putative regulatory sequences. We have now asked whether mammary-specific induction of these genes can be linked to the presence of additional transcription factors, which would act in concert with STAT5. RNA-seq analysis at parturition identified 370 genes that were under NFIB control. Notably, 75% of these genes, encoding proteins linked to the differentiation of mammary epithelium, were also regulated by STAT5. This study demonstrates that the STAT5-NFIB module is an essential part of genes that define differentiation and function of the mammary gland. Expression profiling by high throughput sequencing in wild-type (WT) and Nfib-null (KO) mammary gland tissues
Project description:Mice deficient for miR-212/132 have been reported to show impaired mammary gland development. However, another miR-212/132-deficient line does not demonstrate any obvious defects in mammary gland organogenesis. The transcriptome analysis in the mammary gland of the previously reported miR-212/132-deficient line by deep RNA-seq revealed significantly deregulated expression of genes flanking Mir-212/132 locus, such as HIC1, implying that the mammary gland phenotype might not be only due to loss of miR-212/132
Project description:Mice deficient for miR-212/132 have been reported to show impaired mammary gland development. However, another miR-212/132-deficient line does not demonstrate any obvious defects in mammary gland organogenesis. The transcriptome analysis in the mammary gland of the previously reported miR-212/132-deficient line by deep RNA-seq revealed significantly deregulated expression of genes flanking Mir-212/132 locus, such as HIC1, implying that the mammary gland phenotype might not be only due to loss of miR-212/132 Mammary gland mRNA profiles of Wild Type and Mir-212/132ILN/ILN mice were generated by deep sequencing using Illumina GAIIx.
Project description:The mammary gland undergoes extensive remodeling between the begin- ning of pregnancy and lactation; this involves cellular processes including cell proliferation, differentiation, and apoptosis, all of which are under the control of numerous regulators. To unravel the role played by miRNA, we describe here 47 new ovine miRNA cloned from mammary gland in early pregnancy displaying strong similari- ties with those already identified in the cow, human, or mouse. A microarray study of miRNA variations in the adult ovine mammary gland during pregnancy and lactation showed that 100 miRNA are regulated according to three principal patterns of expression: a de- crease in early pregnancy, a peak at midpregnancy, or an increase throughout late pregnancy and lactation. One miRNA displaying each pattern (miR-21, miR-205, and miR-200b) was analyzed by qRT- PCR. Variations in expression were confirmed for all three miRNA. Using in situ hybridization, we detected both miR-21 and miR-200 in luminal mammary epithelial cells when expressed, whereas miR-205 was expressed in basal cells during the first half of pregnancy and then in luminal cells during the second half. We therefore conclude that miR-21 is strongly expressed in the luminal cells of the normal mammary gland during early pregnancy when extensive cell prolif- eration occurs. In addition, we show that miR-205 and miR-200 are coexpressed in luminal cells, but only during the second half of pregnancy. These two miRNA may cooperate to maintain epithelial status by repressing an EMT-like program, to achieve and preserve the secretory phenotype of mammary epithelial cells.