Notch Lineages and Activity in Intestinal Stem Cells Determined by a New Set of Knock-In Mice

Fre, Silvia; Hannezo, Édouard; Sale, Sanja; Huyghe, Mathilde; Lafkas, Daniel; Kissel, Holger; Louvi, Angeliki; Greve, Jeffrey M.; Louvard, Daniel; Artavanis‐Tsakonas, Spyros

doi:10.1371/journal.pone.0025785

Cited by 125 publications

(144 citation statements)

References 39 publications

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“…Hes1-CreER T2 mice (Kopinke et al, 2011) were provided by Dr Charles Murtaugh at the University of Utah. Hes1-GFP mice (Fre et al, 2011) and Hes1 f/f mice (Revollo et al, 2013) were kindly provided by Dr Spyros Artavanis-Tsakonas at Harvard College and Dr John A. Cidlowski at National Institute of Environmental Health Sciences, respectively. Female mice were housed with male mice overnight and checked for the presence of a vaginal plug the next morning.…”

Section: Animalsmentioning

confidence: 99%

Mapping lineage progression of somatic progenitor cells in the mouse fetal testis

2016

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Testis morphogenesis is a highly orchestrated process involving lineage determination of male germ cells and somatic cell types. Although the origin and differentiation of germ cells are known, the developmental course specific for each somatic cell lineage has not been clearly defined. Here, we construct a comprehensive map of somatic cell lineage progression in the mouse testis. Both supporting and interstitial cell lineages arise from WT1 + somatic progenitor pools in the gonadal primordium. A subpopulation of WT1 + progenitor cells acquire SOX9 expression and become Sertoli cells that form testis cords, whereas the remaining WT1 + cells contribute to progenitor cells in the testis interstitium. Interstitial progenitor cells diversify through the acquisition of HES1, an indication of Notch activation, at the onset of sex determination. HES1 + interstitial progenitors, through the action of Sertoli cell-derived Hedgehog signals, become positive for GLI1. The GLI1 + interstitial cells eventually develop into two cell lineages: steroid-producing fetal Leydig cells and non-steroidogenic cells. The fetal Leydig cell population is restricted by Notch2 signaling from the neighboring somatic cells. The non-steroidogenic progenitor cells retain their undifferentiated state during fetal stage and become adult Leydig cells in post-pubertal testis. These results provide the first lineage progression map that illustrates the sequential establishment of somatic cell populations during testis morphogenesis.

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Section: Animalsmentioning

confidence: 99%

Mapping lineage progression of somatic progenitor cells in the mouse fetal testis

2016

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“…To test whether THs could modulate the Notch pathway, we used Hes1-EmGFP SAT Notch-reporter mice (Fre et al, 2011b) to analyze the responsiveness of the transgene to alterations in TH levels. Notably, GFP expression in these mice mirrors that of Hes1, a known Notch target gene.…”

Section: Ths Activate the Notch Pathway In Vivo And In Vitromentioning

confidence: 99%

“…This allowed us to analyze the relationship between Jag1-expressing cells and GFP/ Hes1-positive cells (i.e. stem and absorptive progenitor cells; Fre et al, 2011b), Dll1-expressing secretory progenitor cells (van Es et al, 2012) and lysozyme-expressing Paneth cells (Fig. 5).…”

Section: Jag1 Expression Pattern In Intestinal Cryptsmentioning

confidence: 99%

The thyroid hormone nuclear receptor TRα1 controls the Notch signaling pathway and cell fate in murine intestine

et al. 2015

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Thyroid hormones control various aspects of gut development and homeostasis. The best-known example is in gastrointestinal tract remodeling during amphibian metamorphosis. It is well documented that these hormones act via the TR nuclear receptors, which are hormone-modulated transcription factors. Several studies have shown that thyroid hormones regulate the expression of several genes in the Notch signaling pathway, indicating a possible means by which they participate in the control of gut physiology. However, the mechanisms and biological significance of this control have remained unexplored. Using multiple in vivo and in vitro approaches, we show that thyroid hormones positively regulate Notch activity through the TRα1 receptor. From a molecular point of view, TRα1 indirectly controls Notch1, Dll1, Dll4 and Hes1 expression but acts as a direct transcriptional regulator of the Jag1 gene by binding to a responsive element in the Jag1 promoter. Our findings show that the TRα1 nuclear receptor plays a key role in intestinal crypt progenitor/stem cell biology by controlling the Notch pathway and hence the balance between cell proliferation and cell differentiation.

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“…Several reporter mice have been generated to address this issue (Basak and Taylor, 2007;Duncan et al, 2005;Fre et al, 2011;Imayoshi et al, 2010;Ohtsuka et al, 2006;Souilhol et al, 2006;Vooijs et al, 2007); however, all of them have certain limitations. Some strategies aim to visualize endogenous Notch receptor activity, in which reporter expression is driven by promoter regions of the Notch target genes Hes1 or Hes5 (Basak and Taylor, 2007;Fre et al, 2011;Imayoshi et al, 2010;Ohtsuka et al, 2006), or by multimerized RBPJj-binding sites (Duncan et al, 2005;Souilhol et al, 2006). Nevertheless, Hes reporters can become activated by alternative signaling pathways and thus are not restricted to Notch-specific activation.…”

mentioning

confidence: 99%

“…The transgenic reporter mouse based on multimerized RBP-jj binding sites is Notch specific, but it is unclear through which of the four receptors the signal is initiated. Notch receptor-specific reporter lines have indeed been generated either by replacing the cytoplasmic domain of Notch1 with a cDNA coding for the cre recombinase (Vooijs et al, 2007) or by knocking in a Cre-ERT2 gene into the ATG of the different Notch receptors (Fre et al, 2011). Although receptor specific, these systems do not discriminate between cells that receive an active Notch signal and cells descending from a Notch signaling precursor.…”

mentioning

confidence: 99%

Generation and characterization of a Notch1 signaling‐specific reporter mouse line

Smith

Claudinot

Lehal

et al. 2012

Genesis

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Signaling through the Notch1 receptor is essential for the control of numerous developmental processes during embryonic life as well as in adult tissue homeostasis and disease. Since the outcome of Notch1 signaling is highly context‐dependent, and its precise physiological and pathological role in many organs is unclear, it is of great interest to localize and identify the cells that receive active Notch1 signals in vivo. Here, we report the generation and characterization of a BAC‐transgenic mouse line, N1‐Gal4VP16, that when crossed to a Gal4‐responsive reporter mouse line allowed the identification of cells undergoing active Notch1 signaling in vivo. Analysis of embryonic and adult N1‐Gal4VP16 mice demonstrated that the activation pattern of the transgene coincides with previously observed activation patterns of the endogenous Notch1 receptor. Thus, this novel reporter mouse line provides a unique tool to specifically investigate the spatial and temporal aspects of Notch1 signaling in vivo. genesis 50:700–710, 2012. © 2012 Wiley Periodicals, Inc.

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Notch Lineages and Activity in Intestinal Stem Cells Determined by a New Set of Knock-In Mice

Cited by 125 publications

References 39 publications

Mapping lineage progression of somatic progenitor cells in the mouse fetal testis

Mapping lineage progression of somatic progenitor cells in the mouse fetal testis

The thyroid hormone nuclear receptor TRα1 controls the Notch signaling pathway and cell fate in murine intestine

Generation and characterization of a Notch1 signaling‐specific reporter mouse line

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