Related Experiment Videos
Disrupted retinal development in the embryonic belly spot and tail mutant mouse
Q Tang1, D S Rice, D Goldowitz
1Center for Neuroscience, University of Tennessee Memphis, 855 Monroe Avenue, Memphis, Tennessee, 38163, USA.
Developmental Biology
|March 2, 1999
Summary
The Belly spot and tail (Bst) mutation causes developmental delays in mouse retinas, impacting cell cycle exit and optic fissure fusion. This research identifies early Bst gene effects on retinal morphogenesis.
Area of Science:
- Developmental Biology
- Genetics
- Ophthalmology
Background:
- The Belly spot and tail (Bst) mutation affects eye, skeleton, and coat development.
- Bst mutations in mice cause retinal colobomas, reduced retinal ganglion cells, and axon misrouting.
- The severity of retinal defects in Bst/+ mice is variable and asymmetric.
Purpose of the Study:
- To investigate the role of the Bst locus in retinal morphogenesis.
- To identify the earliest observable defects in the developing Bst/+ retina.
- To understand the cellular mechanisms underlying Bst-associated retinal abnormalities.
Main Methods:
- Examined retinas of Bst/+ and wildtype (+/+) littermates from embryonic day 9.5 (E9.5) to E13.5.
- Measured retinal size, cell density, cell death, mitotic index, and cell birth index.
- Analyzed optic fissure fusion and cell cycle exit timing.
Main Results:
- Bst/+ retinas showed delayed development by E10.5, being smaller than wildtype.
- Optic fissure fusion was delayed in Bst/+ mutants.
- A significant lag in retinal cell exit from the mitotic cycle was observed, without changes in proliferation or cell death rates.
Conclusions:
- The Bst mutation likely regulates retinal cell differentiation, leading to developmental delays.
- Variability in structural defects, like optic fissure fusion issues, may reflect the extent of developmental delay.
- Early identification of Bst effects provides insights into retinal morphogenesis and mutation-related defects.