BCAS2 is essential for Drosophila viability and functions in pre-mRNA splicing
- Po-Han Chen1,
- Chia-I Lee1,
- Yu-Tzu Weng1,
- Woan-Yuh Tarn2,
- Yeou-Ping Tsao3,
- Ping-Chang Kuo1,
- Pang-Hung Hsu4,5,
- Chu-Wei Huang1,
- Chiun-Sheng Huang6,
- Hsiu-Hsiang Lee7,
- June-Tai Wu7,8 and
- Show-Li Chen1,9
- 1Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
- 2Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan
- 3Department of Ophthalmology, Mackay Memorial Hospital, Taipei 104, Taiwan
- 4Department of Life Science, College of Life Sciences, National Taiwan Ocean University, Keelung 202, Taiwan
- 5Institute of Bioscience and Biotechnology, College of Life Sciences, National Taiwan Ocean University, Keelung 202, Taiwan
- 6Department of Surgery, College of Medicine, National Taiwan University and Hospital, Taipei 100, Taiwan
- 7Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan
- 8Department of Medical Research, National Taiwan University Hospital, Taipei 100, Taiwan
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.
Keywords
Footnotes
-
↵9 Corresponding author
E-mail showlic{at}ntu.edu.tw
- Received June 10, 2012.
- Accepted November 14, 2012.
- Copyright © 2013 RNA Society
