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Related Concept Videos

Gap Junctions01:27

Gap Junctions

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The cytoplasm of adjacent animal cells can exchange small molecules, ions, and secondary messengers via the communication channels which form the gap junctions. These junctions comprise a few hundred to thousands of molecular channels, each made of two halves, called the connexon hemichannel. A connexon is a hexamer of six transmembrane connexin proteins, which assemble radially, thus forming a pore or channel in the center. One connexon hemichannel docks with a corresponding connexon on the...
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Gap Junctions01:37

Gap Junctions

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Multicellular organisms employ a variety of ways for cells to communicate with each other. Gap junctions are specialized proteins that form pores between neighboring cells in animals, connecting the cytoplasm between the two, and allowing for the exchange of molecules and ions. They are found in a wide range of invertebrate and vertebrate species, mediate numerous functions including cell differentiation and development, and are associated with numerous human diseases, including cardiac and...
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P-N junction01:11

P-N junction

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A p-n junction is formed when p-type and n-type semiconductor materials are joined together. At the interface of the p-n junction, holes from the p-side and electrons from the n-side begin to diffuse into the opposite sides due to the concentration gradient. This diffusion of carriers leads to a region around the junction where there are no free charge carriers, known as the depletion region. The charge density within the depletion region for the n-side and p-side can be described by the...
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The Neuromuscular Junction01:19

The Neuromuscular Junction

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The nervous system consists of complex motor neuron circuits, including upper motor neurons originating from the cerebral cortex and lower motor neurons starting in the spinal cord, coordinating both voluntary and involuntary movements. Among these, somatic motor neurons activate skeletal muscles and are classified into alpha, beta, and gamma types. Alpha neurons are vital for voluntary movement coordination, while gamma neurons adjust muscle spindle sensitivity, and the function of beta...
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Anchoring Junctions01:03

Anchoring Junctions

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Anchoring junctions are multiprotein complexes that help cells connect to other cells and the extracellular matrix. Anchoring junctions are present on the lateral and basal surfaces of cells, providing strong and flexible connections. Focal adhesions are often formed due to cell interactions with the ECM substrata, which initiate signal transduction via kinase cascades and other mechanisms. Together, they provide stability and tissue integrity. There are three types of anchoring junctions:...
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Adherens Junctions01:24

Adherens Junctions

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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
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Recording Gap Junction Current from Xenopus Oocytes
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The connexin 46 mutant (V44M) impairs gap junction function causing congenital cataract.

Lijuan Chen1, Dongmei Su, Sijia Li

  • 1Department of Ophthalmology, Hongqi Hospital of Mudanjiang Medical College, Mudanjiang 157000, Heilongjiang Province, People's Republic of China. hushanshan19830219@126.com.

Journal of Genetics
|January 12, 2018
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Summary

A connexin 46 (Cx46) mutation (V44M) causes congenital cataracts by impairing gap junction plaque formation and intercellular communication. This study investigates the V44M mutant

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Genetics

Background:

  • Connexin 46 (Cx46) is vital for lens homeostasis and transparency through gap junction channels.
  • A missense mutation (p.V44M) in Cx46 has been identified in a congenital cataract family.

Purpose of the Study:

  • To investigate the pathogenic mechanisms of the Cx46 V44M mutation in congenital cataracts.
  • To analyze the effects of the Cx46 V44M mutation on gap junction formation and function.

Main Methods:

  • Constructed and expressed wild-type (wt) and V44M mutant Cx46 in Hela cells.
  • Utilized Western blotting, fluorescence microscopy, and scrape loading dye transfer assays.
  • Analyzed protein expression, subcellular localization, plaque formation, and intercellular communication.

Main Results:

  • Both wt-Cx46 and Cx46 V44M localized to the plasma membrane with similar expression levels.
  • Cx46 V44M significantly reduced gap junction plaque formation and Triton X-100 insoluble complex formation.
  • Cells expressing Cx46 V44M exhibited reduced dye transfer, indicating impaired gap junction intercellular communication.

Conclusions:

  • The human Cx46 V44M mutant causes cataracts by disrupting gap junction plaque assembly.
  • The mutation leads to aberrant gap junction channel function and impaired intercellular communication in the lens.
  • Cx46 V44M is a pathogenic mutation contributing to congenital cataracts through disruption of lens cell communication.