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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

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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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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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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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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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Analysis of Zebrafish Kidney Development with Time-lapse Imaging Using a Dissecting Microscope Equipped for Optical Sectioning
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Atmin mediates kidney morphogenesis by modulating Wnt signaling.

Paraskevi Goggolidou1, Nazreen F Hadjirin2, Aggie Bak3

  • 1Leukocyte Biology, National Heart and Lung Institute, Imperial College London, London SW7 2AZ, UK c.dean@imperial.ac.uk p.goggolidou@open.ac.uk.

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Summary

The DNA damage protein Atmin is essential for kidney development. It influences Wnt signaling pathways, impacting kidney tubule formation and potentially contributing to renal diseases.

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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Atmin (Asciz) is a DNA damage protein and transcription factor crucial for lung tubulogenesis and ciliogenesis.
  • Renal ciliary dysfunction is linked to cystic kidney disease, highlighting the importance of kidney tubular development.

Purpose of the Study:

  • To investigate the role of Atmin in kidney development using the Atmin mouse mutant Gasping6 (Gpg6).
  • To elucidate the molecular mechanisms by which Atmin influences kidney development and Wnt signaling.

Main Methods:

  • Analysis of kidney development in Atmin(Gpg6/Gpg6) mice.
  • Assessment of gene expression, cytoskeletal organization, and Wnt signaling pathway components.
  • Genetic interaction studies between Atmin and Vangl2 mutants.

Main Results:

  • Atmin deficiency severely disrupted kidney development, reducing branching morphogenesis and epithelial structures.
  • Altered cytoskeletal organization and modulation of Wnt signaling pathway molecules (β-catenin, Daam2, Vangl2) were observed.
  • Atmin(Gpg6/Gpg6) mice exhibited shortened body axis and mis-oriented cell division, characteristic of PCP pathway mutants.
  • A genetic interaction between Atmin and Vangl2 was identified.

Conclusions:

  • Atmin is critical for normal kidney development.
  • Atmin acts as a novel effector molecule in the non-canonical Wnt/planar cell polarity (PCP) pathway.
  • The findings provide insights into the pathobiology of renal diseases and identify Atmin as a potential therapeutic target.