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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 TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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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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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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Related Experiment Video

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Fat4-Dchs1 signalling controls cell proliferation in developing vertebrae.

Anna Kuta1, Yaopan Mao2, Tina Martin1

  • 1Department of Craniofacial Development and Stem Cell Biology, King's College London, Dental Institute, Guy's Tower, Floor 27, London SE1 9RT, UK.

Development (Cambridge, England)
|July 7, 2016
PubMed
Summary

Fat4 and Dchs1 signaling are crucial for vertebral development in mice by controlling cell proliferation, not planar cell polarity or the Hippo pathway. These findings reveal a novel mechanism for vertebrate formation.

Keywords:
ChondrocyteDchs1Fat4MouseSomiteTaz (Wwtr1)VertebraeYap1

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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Protocadherins Fat4 and Dchs1 form a receptor-ligand pair regulating development.
  • Fat4-Dchs1 signaling is implicated in planar cell polarity (PCP) and Hippo pathway effectors Yap/Taz.
  • Vertebral defects in Fat4/Dchs1 mutants suggest altered cell polarity or proliferation.

Purpose of the Study:

  • Investigate the role of Fat4-Dchs1 signaling in vertebral development.
  • Clarify the link between Fat4-Dchs1, PCP, and the Hippo pathway in vertebrae.
  • Identify the precise cellular defect in Fat4/Dchs1 mutant mice.

Main Methods:

  • Analysis of Fat4(-/-) and Dchs1(-/-) mutant mice.
  • Examination of somite and sclerotome specification and chondrogenesis.
  • Assessment of cell polarity and proliferation in the sclerotome.
  • Analysis of Fat4;Yap and Fat4;Taz double mutants.

Main Results:

  • Vertebrae in Fat4/Dchs1 mutants exhibit midline splitting and fusion.
  • Sclerotome specification and early chondrogenesis are normal.
  • The primary defect is decreased sclerotome cell proliferation, leading to improper vertebral condensation.
  • Fat4-Dchs1 regulates vertebral development independently of Yap and Taz.

Conclusions:

  • Fat4-Dchs1 signaling is essential for regulating cell proliferation during vertebral development.
  • The mechanism of Fat4-Dchs1 action in vertebrae is distinct from its roles in PCP and Hippo signaling.
  • Novel mechanisms of Fat4-Dchs1 signaling have evolved for vertebral development.