Cytoarchitectural changes in the developing cerebellar cortex of the laggard mutant mouse
Junaedy Yunus1, Tomiyoshi Setsu2, Satoshi Kikkawa2
1Department of Anatomy, Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Narra J
|September 15, 2025
Summary
The Kif14 gene mutation in laggard mice disrupts cerebellar cortex development, causing cell death and disorganized layers. This Kif14 mutation leads to severe cerebellar structural abnormalities in mice.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- The laggard (lag) mouse model, caused by a Kif14 gene mutation, exhibits neurological deficits including ataxia and premature death.
- Kif14 mutations disrupt the layered architecture of multiple brain regions, including the cerebellar cortex.
Purpose of the Study:
- To investigate the specific effects of the Kif14 mutation on the cellular development and cytoarchitecture of the cerebellar cortex.
Main Methods:
- Hematoxylin-eosin staining and immunohistochemistry to assess cerebellar cortex morphology.
- TUNEL and BrdU assays to evaluate apoptotic and proliferating cells.
- Macroscopic and microscopic analysis of wild-type and lag mutant cerebellums.
Main Results:
- Lag mutant cerebellums are significantly smaller with disorganized cerebellar cortex cytoarchitecture.
- Reduced granule cell numbers and underdeveloped Purkinje cell dendritic arborization were observed.
- Increased apoptosis in the external granular layer and evidence of disrupted cell division (multi-nucleated Purkinje cells) were noted.
Conclusions:
- The Kif14 mutation leads to significant structural abnormalities in the developing cerebellar cortex, characterized by impaired cell proliferation and increased cell death.
- Kif14 plays critical roles in cerebellar cortex development, including cell division and the formation of laminated structures.
- These findings highlight the multifaceted roles of the Kif14-encoded protein in brain development and myelination.
