端粒酶
RNA剪接
选择性拼接
计算生物学
生物
细胞生物学
遗传学
基因
核糖核酸
外显子
作者
Mandy S. Wong,Ling Chen,C. M. Foster,Radhika Kainthla,Jerry W. Shay,Woodring E. Wright
出处
期刊:Cell Reports
[Cell Press]
日期:2013-04-01
卷期号:3 (4): 1028-1035
被引量:60
标识
DOI:10.1016/j.celrep.2013.03.011
摘要
Telomerase is present in human cancer cells but absent in most somatic tissues. The messenger RNA of human telomerase (hTERT) is alternatively spliced into mostly nonfunctional products. We sought to understand splicing so that we could decrease functional splice isoforms to reduce telomerase activity in order to complement direct enzyme inhibition. Unexpectedly, minigenes containing hTERT exons 5–10 flanked by 150–300 bp intronic sequences did not produce alternative splicing. A 1.1 kb region of 38 bp repeats ∼2 kb from the exon 6/intron junction restored the exclusion of exons 7 and 8. An element within intron 8, also >1 kb from intron/exon junctions, modulated this effect. Transducing an oligonucleotide complementary to this second element increased nonfunctional hTERT messenger RNA from endogenous telomerase. These results demonstrate the potential of manipulating hTERT splicing for both chemotherapy and regenerative medicine and provide specific sequences deep within introns that regulate alternative splicing in mammalian cells by mechanisms other than the introduction of cryptic splice sites.
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