Author:
Chen Po-Han,Lee Chia-I,Weng Yu-Tzu,Tarn Woan-Yuh,Tsao Yeou-Ping,Kuo Ping-Chang,Hsu Pang-Hung,Huang Chu-Wei,Huang Chiun-Sheng,Lee Hsiu-Hsiang,Wu June-Tai,Chen Show-Li
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.
Publisher
Cold Spring Harbor Laboratory
Cited by
19 articles.
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