scholarly journals Elf5 Regulates Mammary Gland Stem/Progenitor Cell Fate by Influencing Notch Signaling

Stem Cells ◽  
2012 ◽  
Vol 30 (7) ◽  
pp. 1496-1508 ◽  
Author(s):  
Rumela Chakrabarti ◽  
Yong Wei ◽  
Rose-Anne Romano ◽  
Christina DeCoste ◽  
Yibin Kang ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Notch Signaling ◽  
Cell Fate ◽  
Progenitor Cell

scholarly journals Alveolar progenitor differentiation and lactation depends on paracrine inhibition of notch via ROBO1/CTNNB1/JAG1

Development ◽  
2021 ◽  
Vol 148 (21) ◽  
Author(s):  
Oscar Cazares ◽  
Sharmila Chatterjee ◽  
Pinky Lee ◽  
Catherine Strietzel ◽  
J. W. Bubolz ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Notch Signaling ◽  
Progenitor Cell ◽  
Tissue Growth ◽  
Basal Cells ◽  
Estrus Cycle ◽  
Regulatory Pathway ◽  
Progenitor Cell Population ◽  
Luminal Compartment ◽  
Notch Activation

ABSTRACT In the mammary gland, how alveolar progenitor cells are recruited to fuel tissue growth with each estrus cycle and pregnancy remains poorly understood. Here, we identify a regulatory pathway that controls alveolar progenitor differentiation and lactation by governing Notch activation in mouse. Loss of Robo1 in the mammary gland epithelium activates Notch signaling, which expands the alveolar progenitor cell population at the expense of alveolar differentiation, resulting in compromised lactation. ROBO1 is expressed in both luminal and basal cells, but loss of Robo1 in basal cells results in the luminal differentiation defect. In the basal compartment, ROBO1 inhibits the expression of Notch ligand Jag1 by regulating β-catenin (CTNNB1), which binds the Jag1 promoter. Together, our studies reveal how ROBO1/CTTNB1/JAG1 signaling in the basal compartment exerts paracrine control of Notch signaling in the luminal compartment to regulate alveolar differentiation during pregnancy.

Modulation of the notch signaling by Mash1 and Dlx1/2regulates sequential specification and differentiation of progenitor cell types in the subcortical telencephalon

Development ◽  
2002 ◽  
Vol 129 (21) ◽  
pp. 5029-5040 ◽  
Author(s):  
Kyuson Yun ◽  
Seth Fischman ◽  
Jane Johnson ◽  
Martin Hrabe de Angelis ◽  
Gerry Weinmaster ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Notch Signaling ◽  
Cell Fate ◽  
Progenitor Cell ◽  
Cell Types ◽  
Cell Fate Specification ◽  
Early Neurogenesis ◽  
Molecular Phenotypes ◽  
Postmitotic Cell ◽  
Homeobox Transcription Factors

Notch signaling has a central role in cell fate specification and differentiation. We provide evidence that the Mash1 (bHLH) andDlx1 and Dlx2 (homeobox) transcription factors have complementary roles in regulating Notch signaling, which in turn mediates the temporal control of subcortical telencephalic neurogenesis in mice. We defined progressively more mature subcortical progenitors (P1, P2 and P3) through their combinatorial expression of MASH1 and DLX2, as well as the expression of proliferative and postmitotic cell markers at E10.5-E11.5. In the absence ofMash1, Notch signaling is greatly reduced and `early' VZ progenitors(P1 and P2) precociously acquire SVZ progenitor (P3) properties. Comparing the molecular phenotypes of the delta-like 1 and Mash1 mutants, suggests that Mash1 regulates early neurogenesis through Notch-and Delta-dependent and -independent mechanisms. While Mash1 is required for early neurogenesis (E10.5), Dlx1 and Dlx2 are required to downregulate Notch signaling during specification and differentiation steps of `late' progenitors (P3). We suggest that alternate cell fate choices in the developing telencephalon are controlled by coordinated functions of bHLH and homeobox transcription factors through their differential affects on Notch signaling.

scholarly journals The Mammary Gland Microenvironment Directs Progenitor Cell FateIn Vivo

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Karen M. Bussard ◽  
Gilbert H. Smith
Keyword(s):  
Mammary Gland ◽  
Epithelial Cell ◽  
Cell Fate ◽  
Progenitor Cell ◽  
Myoepithelial Cells ◽  
Mammary Epithelial ◽  
Terminal End Buds ◽  
Mammary Stem ◽  
Luminal And Myoepithelial Cells

The mammary gland is a unique organ that continually undergoes postnatal developmental changes. In mice, the mammary gland is formed via signals from terminal end buds, which direct ductal growth and elongation. Intriguingly, it is likely that the entire cellular repertoire of the mammary gland is formed from a single antecedent cell. Furthermore, in order to produce progeny of varied lineages (e.g., luminal and myoepithelial cells), signals from the local tissue microenvironment influence mammary stem/progenitor cell fate. Data have shown that cells from the mammary gland microenvironment reprogram adult somatic cells from other organs (testes, nerve) into cells that produce milk and express mammary epithelial cell proteins. Similar results were found for human tumorigenic epithelial carcinoma cells. Presently, it is unclear how the deterministic power of the mammary gland microenvironment controls epithelial cell fate. Regardless, signals generated by the microenvironment have a profound influence on progenitor cell differentiationin vivo.

scholarly journals Macrophage-derived Wnt opposes Notch signaling to specify hepatic progenitor cell fate in chronic liver disease

2012 ◽  
Vol 18 (4) ◽  
pp. 572-579 ◽  
Author(s):  
Luke Boulter ◽  
Olivier Govaere ◽  
Tom G Bird ◽  
Sorina Radulescu ◽  
Prakash Ramachandran ◽  
...  
Keyword(s):  
Liver Disease ◽  
Notch Signaling ◽  
Chronic Liver Disease ◽  
Cell Fate ◽  
Progenitor Cell ◽  
Chronic Liver ◽  
Hepatic Progenitor Cell

scholarly journals Role of Jagged1-mediated Notch Signaling Activation in the Differentiation and Stratification of the Human Limbal Epithelium

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1945
Author(s):  
Sheyla González ◽  
Maximilian Halabi ◽  
David Ju ◽  
Matthew Tsai ◽  
Sophie X. Deng
Keyword(s):  
Notch Signaling ◽  
Progenitor Cell ◽  
Basal Layer ◽  
Notch Signaling Pathway ◽  
Basal Cells ◽  
Proliferation Markers ◽  
Limbal Epithelium ◽  
Asymmetric Divisions ◽  
Signaling Activation

The Notch signaling pathway plays a key role in proliferation and differentiation. We investigated the effect of Jagged 1 (Jag1)-mediated Notch signaling activation in the human limbal stem/progenitor cell (LSC) population and the stratification of the limbal epithelium in vitro. After Notch signaling activation, there was a reduction in the amount of the stem/progenitor cell population, epithelial stratification, and expression of proliferation markers. There was also an increase of the corneal epithelial differentiation. In the presence of Jag1, asymmetric divisions were decreased, and the expression pattern of the polarity protein Par3, normally present at the apical-lateral membrane of basal cells, was dispersed in the cells. We propose a mechanism in which Notch activation by Jag1 decreases p63 expression at the basal layer, which in turn reduces stratification by decreasing the number of asymmetric divisions and increases differentiation.

scholarly journals Notch Signaling Regulation in HCC: From Hepatitis Virus to Non-Coding RNAs

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 521
Author(s):  
Catia Giovannini ◽  
Francesca Fornari ◽  
Fabio Piscaglia ◽  
Laura Gramantieri
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Hepatitis Virus ◽  
Notch Pathway ◽  
Notch Receptor ◽  
Gamma Secretase ◽  
Stem Cell Maintenance ◽  
Pathway Activation ◽  
Promising Therapeutic Approach ◽  
Conserved Genes

The Notch family includes evolutionary conserved genes that encode for single-pass transmembrane receptors involved in stem cell maintenance, development and cell fate determination of many cell lineages. Upon activation by different ligands, and depending on the cell type, Notch signaling plays pleomorphic roles in hepatocellular carcinoma (HCC) affecting neoplastic growth, invasion capability and stem like properties. A specific knowledge of the deregulated expression of each Notch receptor and ligand, coupled with resultant phenotypic changes, is still lacking in HCC. Therefore, while interfering with Notch signaling might represent a promising therapeutic approach, the complexity of Notch/ligands interactions and the variable consequences of their modulations raises concerns when performed in undefined molecular background. The gamma-secretase inhibitors (GSIs), representing the most utilized approach for Notch inhibition in clinical trials, are characterized by important adverse effects due to the non-specific nature of GSIs themselves and to the lack of molecular criteria guiding patient selection. In this review, we briefly summarize the mechanisms involved in Notch pathway activation in HCC supporting the development of alternatives to the γ-secretase pan-inhibitor for HCC therapy.

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