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2009年学术活动

生物物理所学术报告:Genome-wide analysis of PTB binding reveals a strategy used by the general splicing repressor to positively or negatively regulate alternative splicing in mammalian cells

发布时间:2009年07月31日

报告题目:Genome-wide analysis of PTB binding reveals a strategy used by the general splicing repressor to positively or negatively regulate alternative splicing in mammalian cells

报 告 人:Yi Zhang, Ph.D., Professor

Department of Biochemistry and Molecular Biology, College of Life Sciences, Wuhan University

地 点:所图书馆二层报告厅

时 间:2009年8月11日(周二)下午3:30

报告摘要:

Recent transcriptome analysis indicates that >90% of human genes undergoes alternative splicing, underscoring the contribution of differential RNA processing to the structural and functional diversity of the proteome in higher eukaryotic cells. The polypyrimidine tract binding protein PTB has been characterized as a general splicing repressor in vitro, but PTB knockdown by RNAi causes both exon inclusion and skipping in vivo. By genome-wide mapping of PTB-RNA interactions and construction of a functional RNA map, we now provide a plausible mechanism for this paradox. We found that PTB binding sites are frequently associated with both the 5’ and 3’ splice sites regardless of whether or not those sites are involved in alternative splicing. About one third of PTB binding events are linked to regulated splicing in the human genome where dominant binding near a competing constitutive splice  site generally induces exoninclusion whereas prevalent binding close to an alternative site often causes exon skipping. We further demonstrated this position-dependent effect by disrupting or creating a PTB binding site on minigene constructs. These findings suggest a novel mechanism for PTB to modulate splice site competition to produce opposite functional outcomes, which may be generally applicable to RNA binding splicing suppressors to positively or negatively regulate alternative splicing in mammalian cells.

报告人简介:Zhang Yi.pdf

 

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