Neural crest motility on fibronectin is regulated by integrin activation
1Department of Neurobiology and Anatomy, University of Utah, School of Medicine, 20 North 1900 East, Salt Lake City, UT 84132-3401, USA.
Experimental Cell Research
|November 27, 2007
Summary
Neural crest cell (NCC) migration on fibronectin depends on integrin receptor regulation. Cranial and trunk NCCs show distinct responses to integrin activation, influencing their motility.
Area of Science:
- Developmental Biology
- Cell Biology
- Biochemistry
Background:
- Cell migration is crucial for embryonic development, particularly for neural crest cells (NCCs).
- While receptor recycling impacts NCC motility on laminin, mechanisms for fibronectin (FN) migration are less understood.
- Integrin receptor affinity modulation is a key cellular motility regulator.
Purpose of the Study:
- To investigate the role of integrin functional regulation in cranial and trunk NCC migration on fibronectin.
- To elucidate the molecular mechanisms governing NCC motility on fibronectin substrates.
Main Methods:
- Culturing cranial and trunk NCCs on fibronectin (FN) and laminin (LM) substrates.
- Utilizing manganese (Mn2+) treatment to activate all surface integrins.
- Analyzing NCC velocity and the distribution/number of activated integrin beta 1 receptors.
Main Results:
- NCC velocity decreased on fibronectin after Mn2+ treatment, but not on laminin.
- Integrin beta 1 receptor distribution was substratum-dependent.
- Cranial NCCs exhibited FN concentration-dependent velocity changes, unlike trunk NCCs.
- Mn2+ treatment differentially affected activated integrin beta 1 distribution and numbers in cranial and trunk NCCs.
Conclusions:
- Cranial and trunk NCCs utilize functional integrin regulation for efficient fibronectin migration.
- Integrin activation and receptor clustering likely determine NCC motility on fibronectin.
- Differential responses suggest distinct regulatory mechanisms between cranial and trunk NCCs on fibronectin.
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