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Related Concept Videos

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Microtubules in Signaling

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The primary cilium, made up of microtubules, acts as antennae on the cell surfaces for relaying external stimuli into the cells. These fine hair-like structures are present, generally one per cell. These are non-motile cilia in a 9+0 microtubules arrangement, where the central pair of microtubules are absent. The primary cilia arise from the basal body embedded in the cell membrane. Intraflagellar transport (IFT) carries requisite proteins from the cytoplasm to the cilium because the primary...
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The ciliary structures were first seen in 1647 by Antonie Leeuwenhoek while observing the protozoans. In lower organisms, these appendages are responsible for cell movement, while in higher organisms, these appendages help in the movement of the extracellular fluids within the body cavities.
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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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Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
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Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
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After budding out from the ER membrane, some COPII vesicles lose their coat and fuse with one another to form larger vesicles and interconnected tubules called vesicular tubular clusters or VTCs. These clusters constitute a compartment at the ER-Golgi interface known as ERGIC (Endoplasmic Reticulum Golgi Intermediate Compartment). The ERGIC is a mobile membrane-bound cargo transport system that sorts proteins secreted from ER and delivers them to the Golgi.
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Related Experiment Video

Updated: Dec 26, 2025

4-Dimensional Imaging of Zebrafish Optic Cup Morphogenesis
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Optic vesicle morphogenesis requires primary cilia.

Luciano Fiore1, Nozomu Takata1, Sandra Acosta2

  • 1Center for Vascular and Developmental Biology, Feinberg Cardiovascular and Renal Research Institute (FCVRRI), Northwestern University, Chicago, IL, USA.

Developmental Biology
|March 15, 2020
PubMed
Summary
This summary is machine-generated.

Arl13b gene mutations disrupt eye development by affecting optic cup orientation and Sonic hedgehog signaling. Restoring Shh pathway signaling via Gli2 deletion rescues these developmental defects.

Keywords:
Arl13bEyeMorphogenesisMouseOptic vesiclePrimary ciliaShh

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Area of Science:

  • Developmental Biology
  • Genetics
  • Ophthalmology

Background:

  • Arl13b regulates ciliogenesis, and its dysfunction is linked to Joubert syndrome.
  • Primary cilia play crucial roles in embryonic development and signaling pathways.

Purpose of the Study:

  • To investigate the role of Arl13b in eye development.
  • To elucidate the molecular mechanisms underlying Arl13b-associated eye abnormalities.

Main Methods:

  • Analysis of Arl13b null mouse embryos.
  • Examination of optic cup morphology and orientation.
  • Investigation of Sonic hedgehog (Shh) signaling pathway activity.
  • Genetic rescue experiments involving Gli2 deletion.

Main Results:

  • Arl13b null embryos exhibit inverted optic cup orientation and disrupted optic vesicle patterning.
  • Loss of Arl13b leads to abnormal expansion of ventral fates and Shh signaling misregulation.
  • Deletion of Gli2, a Shh effector, rescues the observed eye phenotype in Arl13b null embryos.

Conclusions:

  • Arl13b plays a critical, previously unrecognized role in eye morphogenesis.
  • Proper eye development relies on Arl13b-mediated regulation of Shh signaling and primary cilia function.
  • This study highlights the importance of cilia in coordinating morphogenetic movements during eye formation.