Faculty Opinions recommendation of MBNL proteins repress ES-cell-specific alternative splicing and reprogramming.

2013 ◽  
Author(s):  
Bill Lowry
Keyword(s):  
Alternative Splicing ◽  
Es Cell ◽  
Specific Alternative

scholarly journals MBNL proteins repress ES-cell-specific alternative splicing and reprogramming

Nature ◽  
2013 ◽  
Vol 498 (7453) ◽  
pp. 241-245 ◽  
Author(s):  
Hong Han ◽  
Manuel Irimia ◽  
P. Joel Ross ◽  
Hoon-Ki Sung ◽  
Babak Alipanahi ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Es Cell ◽  
Specific Alternative

scholarly journals Repression of Prespliceosome Complex Formation at Two Distinct Steps by Fox-1/Fox-2 Proteins

2008 ◽  
Vol 28 (17) ◽  
pp. 5507-5516 ◽  
Author(s):  
Hua-Lin Zhou ◽  
Hua Lou
Keyword(s):  
Alternative Splicing ◽  
Complex Formation ◽  
Biochemical Analysis ◽  
Expression Control ◽  
Regulatory Strategy ◽  
Gene Expression Control ◽  
Splicing Regulator ◽  
Specific Alternative ◽  
Novel Strategy ◽  
Robust Regulation

ABSTRACT Precise and robust regulation of alternative splicing provides cells with an essential means of gene expression control. However, the mechanisms that ensure the tight control of tissue-specific alternative splicing are not well understood. It has been demonstrated that robust regulation often results from the contributions of multiple factors to one particular splicing pathway. We report here a novel strategy used by a single splicing regulator that blocks the formation of two distinct prespliceosome complexes to achieve efficient regulation. Fox-1/Fox-2 proteins, potent regulators of alternative splicing in the heart, skeletal muscle, and brain, repress calcitonin-specific splicing of the calcitonin/CGRP pre-mRNA. Using biochemical analysis, we found that Fox-1/Fox-2 proteins block prespliceosome complex formation at two distinct steps through binding to two functionally important UGCAUG elements. First, Fox-1/Fox-2 proteins bind to the intronic site to inhibit SF1-dependent E′ complex formation. Second, these proteins bind to the exonic site to block the transition of E′ complex that escaped the control of the intronic site to E complex. These studies provide evidence for the first example of regulated E′ complex formation. The two-step repression of presplicing complexes by a single regulator provides a powerful and accurate regulatory strategy.

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