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Musashi and seven in absentia downregulate Tramtrack through distinct mechanisms in Drosophila eye development
1Division of Neuroanatomy (D12), Department of Neuroscience, Biomedical Research Center, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, Japan.
Abstract:
We have examined the roles played by the Drosophila neural RNA-binding protein Musashi (MSI) in eye development. MSI expression was observed in the nuclei of all photoreceptor cells (R1-R8). Although a msi loss-of-function mutation resulted in only weak abnormalities in photoreceptor differentiation, we found that the msi eye phenotype was significantly enhanced in a seven in absentia (sina) background. sina is known to be involved in the degradation of the Tramtrack (TTK) protein, leading to the specification of the R7 fate. We demonstrated that MSI also functions to regulate TTK expression. The sina msi mutants showed significantly high ectopic expression of TTK69 and failure in the determination of the R1, R6, and R7 fates. Other photoreceptor cells also failed to differentiate with abnormalities occurring late in the differentiation process. These results suggest that MSI and SINA function redundantly to downregulate TTK in developing photoreceptor cells.
Insights
The Drosophila neural RNA-binding protein Musashi (MSI) and seven in absentia (SINA) redundantly regulate Tramtrack (TTK) protein levels during eye development. This ensures proper photoreceptor cell fate determination.
Area of Science:
- Developmental biology
- Neuroscience
- Genetics
Background:
- The Drosophila neural RNA-binding protein Musashi (MSI) plays roles in cell differentiation.
- Seven in absentia (SINA) is crucial for R7 photoreceptor cell fate specification by degrading the Tramtrack (TTK) protein.
Purpose of the Study:
- To investigate the role of MSI in Drosophila eye development.
- To elucidate the relationship between MSI and SINA in photoreceptor differentiation.
Main Methods:
- Analysis of msi loss-of-function mutations in Drosophila.
- Examination of genetic interactions between msi and sina mutants.
- Assessment of TTK protein expression in developing photoreceptor cells.
Main Results:
- MSI is expressed in all photoreceptor nuclei (R1-R8).
- msi mutations enhance the eye phenotype in a sina background, leading to ectopic TTK69 expression.
- sina msi mutants exhibit defects in R1, R6, and R7 photoreceptor cell fate determination and differentiation.
Conclusions:
- MSI, along with SINA, functions to downregulate TTK expression.
- MSI and SINA act redundantly to control TTK levels, ensuring proper photoreceptor differentiation in Drosophila.
- This study highlights a conserved mechanism for RNA-binding proteins in regulating developmental gene expression.