Abstract
The T-box transcription factor mab-9 has been shown to be required for the correct fate of the male-specific blast cells B and F, normal posterior hypodermal morphogenesis, and for the correct axon migration of motor neurons that project circumferential commissures to dorsal muscles. In this study, an RNAi screen designed to identify upstream transcriptional regulators of mab-9 showed that silencing of unc-4 (encoding a paired-class homeodomain protein) increases mab-9::gfp expression in the nervous system, specifically in posterior DA motor neurons. Over-expression of unc-4 from a heat-shock promoter has the opposite effect, causing repression of mab-9 in various cells. We find that mab-9 expression in unc-37 mutants is also elevated in DA motor neurons, consistent with known roles for UNC-37 as a co-repressor with UNC-4. These results identify mab-9 as a novel target of the UNC-4/UNC-37 repressor complex in motor neurons, and suggest that mis-expression of mab-9 may contribute to the neuronal wiring defects in unc-4 and unc-37 mutants.
Originalsprog | Engelsk |
---|---|
Tidsskrift | Mechanisms of Development |
Vol/bind | 128 |
Udgave nummer | 1-2 |
Sider (fra-til) | 49-58 |
Antal sider | 10 |
ISSN | 0925-4773 |
DOI | |
Status | Udgivet - jan. 2011 |
Emneord
- Animals
- Caenorhabditis elegans
- Caenorhabditis elegans Proteins
- Green Fluorescent Proteins
- Homeodomain Proteins
- Male
- Motor Neurons
- Mutation
- Nuclear Proteins
- Protein Binding
- RNA Interference
- Recombinant Fusion Proteins
- Repressor Proteins
- Transcription Factors