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Transcriptional landscapes underlying Notch-induced lineage conversion and reprogramming of mammary cells

ABSTRACT: Transcriptional landscapes underlying Notch-induced lineage conversion and reprogramming of mammary cells

PROVIDER: PRJNA1118799 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29251500.fastq.gz	Fastqsanger.gz
	SRR29251600.fastq.gz	Fastqsanger.gz
	SRR29251700_1.fastq.gz	Fastqsanger.gz
	SRR29251700_2.fastq.gz	Fastqsanger.gz
	SRR29251800.fastq.gz	Fastqsanger.gz

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Transcriptional landscapes underlying Notch-induced lineage conversion and plasticity of mammary basal cells

Project description:The mammary epithelium derives from multipotent mammary stem cells (MaSCs) that engage into differentiation during embryonic development. However, adult MaSCs maintain the ability to reactivate multipotency in non-physiological contexts. We previously reported that Notch1 activation in committed basal cells triggers a basal-to-luminal cell fate switch in the mouse mammary gland. Here, we report conservation of this mechanism and found that in addition to the mammary gland, constitutive Notch1 signaling induces a basal-to-luminal cell fate switch in adult cells of the lacrimal gland, the salivary gland, and the prostate. Since the lineage transition is progressive in time, we performed single-cell transcriptomic analysis on index-sorted mammary cells at different stages of lineage conversion, generating a temporal map of changes in cell identity. Combining single-cell analyses with organoid assays, we demonstrate that cell proliferation is indispensable for this lineage conversion. We also reveal the individual transcriptional landscapes underlying the cellular plasticity switching of committed mammary cells in vivo with spatial and temporal resolution. Given the roles of Notch signaling in cancer, these results may help to better understand the mechanisms that drive cellular transformation.

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Transcriptional landscapes underlying Notch-induced lineage conversion and reprogramming of mammary cells

Project description:Ectopic activation of NOTCH1 (N1ICD) in adult unipotent basal cells induced a cell fate switch to luminal lineage. We investigated the transcriptomic evolution of the during this transition.

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Project description:Luminal to basal transition in mammary gland is accompanied by the changes of epithelial cell lineage plasticity, however, the underlying mechanism remains elusive. Here, we demonstrated that loss of the scaffold protein FRMD3 in breast cancer predicts poor outcomes. Knockout of Frmd3 inhibits mammary gland lineage development and induces mammary epithelium cells (MECs) stemness, and later on emerge of TNBC. Loss of Frmd3 in PyMT mice results in luminal to basal phenotype transition. Single- MEC mRNA sequencing analysis indicated that knockout of Frmd3 corresponds to inhibition of Notch signaling pathway. Mechanistically, FRMD3 assists Dishevelled-2 degradation via enhancing its interaction with the deubiquitinase USP9x. FRMD3 also interrupts the interaction of Dishevelled-2 with CK1, FOXK1, FOXK2 and NICD, causing a decrease in Dishevelled-2 phosphorylation, entry into the nucleus and impairing the Notch-dependent luminal epithelial lineage plasticity in MECs respectively. Taken together, FRMD3 is a tumor suppressor and an endogenous activator of the Notch signaling pathway that regulates mammary epithelial cell lineage plasticity.

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Project description:Pregnancy has been shown to decrease the risk of mammary carcinogenesis in human rretrospective epidemiological studies. In rodents, pregnancy prior to carcinogen administration or after carcinogen challenge has also been shown to reduce the incidence of palpable carcinomas. In this study our objective to determine the underlying genomic signature of the pregnancy and reproductive hormones on the mammary gland that contribute to the protection against mammary gland carcinogenesis. We used the rat microarray technology to observe total transcriptome changes after the pregnancy and exogenous reproductive hormone stimulation of the mammary gland.

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