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Follow that cell: Leukocyte migration in L-plastin mutant zebrafish
John B Linehan1, Jose Lucas Zepeda1, Taylor A Mitchell1
1Department of Biological Sciences, DePaul University, Chicago, USA.
Cytoskeleton (Hoboken, N.J.)
|July 11, 2022
Summary
Zebrafish lacking L-plastin (LCP1) show impaired macrophage migration and morphology, impacting immune cell function. This actin-bundling protein is crucial for macrophage polarity and directed movement during wound response.
Area of Science:
- Cell Biology
- Immunology
- Developmental Biology
Background:
- Actin assemblies are crucial for motile cells like leukocytes.
- L-plastin (LCP1) is a leukocyte-specific actin-bundling protein influencing immune cell migration.
- Previous studies showed zebrafish lacking LCP1 had reduced survival, suggesting immune system impact.
Purpose of the Study:
- To investigate the role of L-plastin in zebrafish neutrophil and macrophage migration and distribution.
- To determine if LCP1 deficiency affects immune cell function in larval zebrafish.
Main Methods:
- Generated CRISPR/Cas9 zebrafish lacking L-plastin (lcp1-/-).
- Examined neutrophil and macrophage distribution and migration in larval zebrafish tails using cell-specific markers.
- Utilized a wound-migration assay to assess cell motility.
Main Results:
- Zebrafish lacking L-plastin showed no gross defects in neutrophil production or migration.
- Macrophage migration to wounds was impaired in LCP1 knockout larvae; they were slower, less directional, and exhibited altered morphology.
- Heterozygous macrophages displayed faster, more directional migration with a streamlined morphology.
Conclusions:
- L-plastin knockout primarily affects macrophage response in larval zebrafish, with potential consequences for organismal immunity.
- Proposed model: Cytoplasmic L-plastin negatively regulates macrophage integrin adhesion and is essential for establishing macrophage polarity during chemokine-induced motility.
