Intestinal development and differentiation

Noah, Taeko K.; Donahue, Bridgitte; Shroyer, Noah F.

doi:10.1016/j.yexcr.2011.09.006

Cited by 305 publications

(259 citation statements)

References 86 publications

Supporting

Mentioning

246

Contrasting

Unclassified

Order By: Relevance

“…Consistent with these results, we measured by RT-qPCR a moderate but significant upregulation of the goblet cell marker Muc2 in NleVilcKO intestines, whereas ChromograninA and Lysozyme mRNA levels were unchanged ( Figure 3b). We found that the local increase in goblet cell number was preceded by the upregulation of Atoh1, a key regulator of secretory cell lineage commitment, 27 and of Spdef, which is required downstream of Atoh1 for goblet cell terminal maturation 28 (Figure 3c). Hes1 expression was unchanged, confirming that the absorptive lineage was not affected by Nle loss of function ( Figure 3c).…”

Section: Resultsmentioning

confidence: 91%

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

et al. 2015

View full text Add to dashboard Cite

International audienceRibosome biogenesis is an essential cellular process. Its impairment is associated with developmental defects and increased risk of cancer. The in vivo cellular responses to defective ribosome biogenesis and the underlying molecular mechanisms are still incompletely understood. In particular, the consequences of impaired ribosome biogenesis within the intestinal epithelium in mammals have not been investigated so far. Here we adopted a genetic approach to investigate the role of Notchless (NLE), an essential actor of ribosome biogenesis, in the adult mouse intestinal lineage. Nle deficiency led to defects in the synthesis of large ribosomal subunit in crypts cells and resulted in the rapid elimination of intestinal stem cells and progenitors through distinct types of cellular responses, including apoptosis, cell cycle arrest and biased differentiation toward the goblet cell lineage. Similar observations were made using the rRNA transcription inhibitor CX-5461 on intestinal organoids culture. Importantly, we found that p53 activation was responsible for most of the cellular responses observed, including differentiation toward the goblet cell lineage. Moreover, we identify the goblet cell-specific marker Muc2 as a direct transcriptional target of p53. Nle-deficient ISCs and progenitors disappearance persisted in the absence of p53, underlying the existence of p53-independent cellular responses following defective ribosome biogenesis. Our data indicate that NLE is a crucial factor for intestinal homeostasis and provide new insights into how perturbations of ribosome biogenesis impact on cell fate decisions within the intestinal epithelium

show abstract

Section: Resultsmentioning

confidence: 91%

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

et al. 2015

View full text Add to dashboard Cite

show abstract

“…1, top). Epigenetic factors are of paramount importance throughout organogenesis, as endoderm-mesoderm interactions have been found to direct the formation of various surface patterns that characterize the adult epithelia [4]. During the first stage of morphogenesis, different rates of cell proliferation in the two layers give rise to residual stresses to promote a mechanical instability, which triggers the occurrence of regional specificities.…”

mentioning

confidence: 99%

Pattern Selection in Growing Tubular Tissues

Ciarletta¹,

Balbi²,

Kuhl³

2014

Phys. Rev. Lett.

111

View full text Add to dashboard Cite

Tubular organs display a wide variety of surface morphologies including circumferential and longitudinal folds, square and hexagonal undulations, and finger-type protrusions. Surface morphology is closely correlated to tissue function and serves as a clinical indicator for physiological and pathological conditions, but the regulators of surface morphology remain poorly understood. Here, we explore the role of geometry and elasticity on the formation of surface patterns. We establish morphological phase diagrams for patterns selection and show that increasing the thickness or stiffness ratio between the outer and inner tubular layers induces a gradual transition from circumferential to longitudinal folding. Our results suggest that physical forces act as regulators during organogenesis and give rise to the characteristic circular folds in the esophagus, the longitudinal folds in the valves of Kerckring, the surface networks in villi, and the crypts in the large intestine.

show abstract

“…Following induction and molecular modeling the endoderm undergoes folding in which the embryonic primary intestine forms. Although the process of endodermic tubulogenesis is still not thoroughly investigated, it is considered to include interaction with the mesenchyme which surrounds it [8]. The process is initiated by invagination in the anterior and posterior end of the embryo called anterior intestinal portal (AIP) and caudal intestinal portal (CIP).…”

Section: Discussionmentioning

confidence: 99%

“…In the early stages of embryogenesis, the gastrointestinal tract is a simple endoblastic tube covered by a layer of mesenchyme. Although the process of endoblastic tubulogenesis is not completely studied, it is presumed that it also includes interaction with the mesenchyme which surrounds it [8]. In mice this process ends on 9 th gestation day [9,10].…”

mentioning

confidence: 99%

Ghrelin As An Ontogenetic Factor And A Gastrointestinal Hormone In The Prenatal And Postnatal Period In Rat

Penkova¹,

Atanassova²,

Georgieva³

et al. 2017

IOSR JDMS

View full text Add to dashboard Cite

gestation day, as well as in the epithelial lining and glands of the stomach and small intestine of one-day-old rats. A ghrelin receptor is expressed in the same periods in endoblastic and myoblastic cells of the developing digestive tube in embryos and fetuses, as well as in the epithelial lining and glands of the stomach and small intestines of newborn rats. Conclusion: Ghrelin-producing cells in the gastro

show abstract

Intestinal development and differentiation

Cited by 305 publications

References 86 publications

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

Pattern Selection in Growing Tubular Tissues

Ghrelin As An Ontogenetic Factor And A Gastrointestinal Hormone In The Prenatal And Postnatal Period In Rat

Contact Info

Product

Resources

About