Abstract
Here, we show that dBCAS2 (CG4980, human Breast Carcinoma Amplified Sequence 2 ortholog) is essential for the viability of Drosophila melanogaster. We find that ubiquitous or tissue-specific depletion of dBCAS2 leads to larval lethality, wing deformities, impaired splicing, and apoptosis. More importantly, overexpression of hBCAS2 rescues these defects. Furthermore, the C-terminal coiled-coil domain of hBCAS2 binds directly to CDC5L and recruits hPrp19/PLRG1 to form a core complex for splicing in mammalian cells and can partially restore wing damage induced by knocking down dBCAS2 in flies. In summary, Drosophila and human BCAS2 share a similar function in RNA splicing, which affects cell viability.
| Original language | English |
|---|---|
| Pages (from-to) | 208-218 |
| Number of pages | 11 |
| Journal | RNA |
| Volume | 19 |
| Issue number | 2 |
| DOIs | |
| State | Published - 02 2013 |
| Externally published | Yes |
Keywords
- BCAS2
- Drosophila
- Prp19 complex
- Splicing
- Viability