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Related Concept Videos

Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

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The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
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The cadherins were one of the first cell adhesion molecules discovered; the term “cadherins”   is based on their calcium-dependent adhering properties. The first cadherins discovered on the epithelial, neuronal, and placental cells were named E-cadherin, P-cadherin, and N-cadherin, respectively. These classical cadherins share sequence and structural similarities. Other cadherins, including those involved in cell signaling, are grouped into non-classical cadherins. This...
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Multiprotein signaling complexes are formed in a dynamic process involving protein-protein interactions at the cytoplasmic domain of transmembrane receptors or enzymatic and non-enzymatic proteins associated with the receptor. These complexes ensure the activation and propagation of intracellular signals that regulate cell functions.
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Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
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Related Experiment Video

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Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration
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Gamma-protocadherins regulate dendrite self-recognition and dynamics to drive self-avoidance.

Samantha Ing-Esteves1, Julie L Lefebvre1

  • 1Program for Neuroscience and Mental Health, Hospital for Sick Children, 686 Bay Street, Toronto, ON M5G 0A4, Canada; Department of Molecular Genetics, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.

Current Biology : CB
|August 30, 2024
PubMed
Summary

Clustered protocadherins (cPcdhs) regulate dendrite self-avoidance in mammalian neurons. This study shows gamma-Pcdhs mediate self-recognition and retraction between sibling dendrites, ensuring proper neuronal morphology.

Keywords:
clustered protocadherinsdendritedendrite dynamicslive imagingmorphogenesisrepulsionretinaself-avoidancestarburst amacrine cellstochastic neurite growth

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Neurons develop specific shapes influenced by cell-surface molecules governing dendrite growth.
  • Dendrite self-avoidance ensures uniform branch distribution within a neuron's territory.
  • Clustered protocadherins (cPcdhs) are implicated in regulating dendrite self-avoidance in mammals.

Purpose of the Study:

  • To directly investigate the dynamics and mechanisms of dendrite self-avoidance during development.
  • To define the role of gamma-Pcdhs (Pcdhgs) in self/non-self-recognition and dendritic arbor patterning in starburst amacrine cells (SACs).

Main Methods:

  • Live imaging and four-dimensional (4D) quantifications of dendrite morphogenesis in mouse retinal SACs.
  • Tracking of dendritic protrusion dynamics, including self-contacting and non-self-contacting events.
  • Analysis of Pcdhg-deficient SACs to assess the impact on self-avoidance mechanisms.

Main Results:

  • Self-contacting dendritic protrusions have longer lifetimes than non-self-contacting ones, with some forming loops.
  • Absence of Pcdhgs significantly reduced retraction of self-contacting protrusions, leading to dendritic bridging and bundling.
  • Non-self-contacting protrusion dynamics remained unaffected in Pcdhg-deficient SACs.

Conclusions:

  • Gamma-Pcdhs (Pcdhgs) actively mediate self-recognition and retraction between contacting sibling dendrites.
  • Self-avoidance, regulated by Pcdhgs, is crucial for shaping stochastic dendritic outgrowth and robust pattern formation in mammalian neurons.