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RNA-seq expression profiling of ductal macrophages and antigen presenting cells from virgin mouse mammary glands

ABSTRACT: Macrophages are diverse immune cells that reside in all tissues to regulate development, function and homeostasis. In the mammary gland, a highly dynamic organ that undergoes dramatic remodeling throughout life, macrophages have been implicated in development and breast tumorigenesis. Ductal macrophages, as opposed to their stromal counterparts, were found to promote ductal morphogenesis during puberty and efficiently phagocytose alveolar cells post-lactation. Within mammary tumors, only ductal macrophages expanded to form a network throughout the tumor, where they also contact intra-tumoral T cells. Furthermore, ductal macrophages accelerated the growth of tumor organoids. Thus, pro-remodeling mammary ductal macrophages represent the normal tissue counterpart of tumor macrophages in an organ that is highly susceptible to oncogenesis. To gain insight into ductal macrophage function, we sorted all antigen presenting cell populations from mouse mammary glands and undertook RNA-seq expression profiling. This showed that ductal macrophages have a distinct expression profile from those of stromal macrophages or dendritic cells from the mammary gland. Results from this data series are presented in Figure 2 of Dawson et al (2020).

ORGANISM(S): Mus musculus

PROVIDER: GSE119869 | GEO | 2020/04/01

REPOSITORIES: GEO

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Project description:Identify gene expression changes in the absence of Plk2 Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Comparison between Plk2 +/+ (n=3) and Plk2 -/- (n=3) mouse mammary epithelial cells

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RNA-seq expression profiling of ductal macrophages and antigen presenting cells from virgin mouse mammary glands

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