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Related Concept Videos

Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Related Experiment Video

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Assaying β-amyloid Toxicity using a Transgenic C. elegans Model
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Wnt Signaling Rescues Amyloid Beta-Induced Gut Stem Cell Loss.

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  • 1Division of Science, Yale-NUS College, Singapore 138527, Singapore.

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This summary is machine-generated.

Wnt signaling activation rescues detrimental effects of amyloid plaques in a Drosophila model, reducing inflammation and improving lifespan. This suggests Wnt pathways may be a therapeutic target for Alzheimer's disease.

Keywords:
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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease is characterized by brain mass reduction and amyloid-β plaques.
  • The precise role of amyloid-β plaques in Alzheimer's progression remains unclear.
  • Optogenetics offers a novel approach to model disease mechanisms.

Purpose of the Study:

  • To investigate the effect of Wnt signaling on amyloid-β in an optogenetic Drosophila gut stem cell model.
  • To elucidate the molecular mechanisms by which Wnt signaling influences amyloid pathology.
  • To explore potential therapeutic targets for Alzheimer's disease.

Main Methods:

  • Development of an optogenetic model to induce amyloid-β intracellular oligomerization.
  • Utilizing Drosophila gut stem cells to study Wnt signaling and amyloid interactions.
  • Analysis of gene expression changes downstream of Wnt activation.

Main Results:

  • Wnt activation demonstrated a rescue of detrimental effects caused by amyloid expression and oligomerization.
  • Gene expression analysis revealed Wnt-mediated changes in aging, protein misfolding, metabolism, and inflammation.
  • Wnt signaling was found to reduce inflammation, partly through the repression of Toll activating factors.
  • Chronic Toll activation negatively impacts lifespan, while inhibiting its upstream activator, Persephone, extends lifespan.

Conclusions:

  • Wnt signaling plays a protective role against amyloid-induced pathology in this model.
  • Wnt activation mitigates Alzheimer's-like pathology by modulating inflammation and related pathways.
  • Lithium's protective effects may be mediated, in part, by Wnt activation and subsequent inflammation inhibition.