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Live-cell Imaging of Sensory Organ Precursor Cells in Intact Drosophila Pupae

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Engineered truncations in the Drosophila mastermind protein disrupt Notch pathway function.

W Helms¹, H Lee, M Ammerman

¹Department of Biology, Emory University, Atlanta, Georgia 30322, USA.

Developmental Biology

|November 5, 1999

Summary

The Drosophila mastermind (mam) gene is crucial for Notch signaling. Truncated Mam proteins act as dominant-negatives, disrupting cell fate and development in various tissues.

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Area of Science:

Developmental Biology
Genetics
Molecular Biology

Background:

The Drosophila mastermind (mam) gene is implicated in the Notch signaling pathway.
Its precise function and site of action in Notch-dependent tissues require further investigation.

Purpose of the Study:

To investigate the function and mechanism of the Drosophila mastermind (mam) gene within the Notch signaling pathway.
To characterize the phenotypes associated with truncated Mam proteins and their role in cell fate specification.

Main Methods:

Construction and expression of truncated Mam proteins in Drosophila imaginal tissues using GAL4-UAS regulation.
Analysis of phenotypes in the notum and wing, including lateral inhibition and cell fate specification.
Genetic modification of phenotypes using mutations in Notch and Wg pathway genes.

Main Results:

Truncated Mam proteins phenocopy Notch pathway loss-of-function mutations.
Expression in the notum disrupts lateral inhibition and sensory organ precursor cell lineage.
Wing expression causes vein thickening, margin defects, and altered gene expression (wg, cut, vg).
Mam truncations act as dominant-negative proteins, with effects suppressed by Delta or activated Notch.

Conclusions:

Truncated Mam proteins lack key effector domains and function as dominant-negatives.
Mastermind likely acts upstream of ligand-receptor interactions in the Notch pathway.
The developed system provides a valuable tool for studying Mam's role in Notch signaling.