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( Namjeong Choi ),( Yongchao Liu ),( Jagyeong Oh ),( Jiyeon Ha ),( Claudia Ghigna ),( Xuexiu Zheng ),( Haihong Shen ) 생화학분자생물학회(구 한국생화학분자생물학회) 2021 BMB Reports Vol.54 No.3
Bcl-x, a member of the Bcl-2 family, plays a key role in apoptosis. Alternative splicing of Bcl-x pre-mRNA through alternative 5’ splice-site selection produces an anti-apoptotic mRNA isoform that includes exon 2b and a pro-apoptotic Bcl-x mRNA isoform that excludes exon 2b. Here we used Bcl-x minigene and identified SRSF2 and SRSF6 as two regulatory factors of 5’ splice-site selection of Bcl-x pre-mRNA. We selected binding clusters closer to 5’ splice-sites from multiple potential binding sites of SRSF2 and SRSF6 to perform loss of functions analysis through site-directed mutagenesis. Our results demonstrated that these mutations did not abolish regulatory functions of SRSF2 or SRSF6, indicating that a single binding motif or a cluster was not a functional target of these proteins in Bcl-x pre-mRNA splicing. Random deletion mutagenesis did not disrupt the role of SRSF2 and SRSF6. Importantly, mutagenesis of 5’ splice-site to a conserved or a weaker score demonstrated that the weaker strength of the target 5’ splice-site or higher strength of the other 5’ splice-site strength limited the role of SRSF2 and SRSF6 in 5’ splice-site activation. [BMB Reports 2021; 54(3): 176-181]
Binding of SRSF4 to a novel enhancer modulates splicing of exon 6 of Fas pre-mRNA
Jang, Ha Na,Liu, Yongchao,Choi, Namjeong,Oh, Jagyeong,Ha, Jiyeon,Zheng, Xuexiu,Shen, Haihong Elsevier 2018 Biochemical and biophysical research communication Vol.506 No.3
<P><B>Abstract</B></P> <P>Alternative splicing of exon 6 in Fas pre-mRNA generates a membrane bound pro-apoptotic isoform or soluble anti-apoptotic isoform. SRSF4 is a member of Arginine-Serine rich (SR) protein family. Here we demonstrate that increased SRSF4 expression stimulates exon 6 inclusion, and that reduced SRSF4 expression promotes exon 6 exclusion. We also show that weaker but not stronger 5’ splice-site strength of exon 6 abolishes the SRSF4 effects on exon 6 splicing. Furthermore, we identified a novel enhancer on exon 6, on which SRSF4 interacts functionally and physically. Our results illustrate a novel regulatory mechanism of Fas pre-mRNA splicing.</P> <P><B>Highlights</B></P> <P> <UL> <LI> SRSF4 expression promotes exon 6 inclusion of Fas pre-mRNA. </LI> <LI> A stronger 5′ splice-site of exon 6 is required for SRSF4-mediated regulation on exon 6 splicing. </LI> <LI> SRSF4 functionally targets GGGGUG RNA sequence on exon 6. </LI> <LI> SRSF4 directly interacts with GGGGUG sequence on exon 6. </LI> </UL> </P>
( Heegyum Moon ),( Ha Na Jang ),( Yongchao Liu ),( Namjeong Choi ),( Jagyeong Oh ),( Jiyeon Ha ),( Hyeon Ho Kim ),( Xuexiu Zheng ),( Haihong Shen ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.11
The Ron proto-oncogene is a human receptor for macrophage-stimulating protein (MSP). The exclusion of exon 11 in alternative splicing generates △RON protein that is constitutively activated. Heterogenous ribonucleaoprotein (hnRNP) C<sub>1</sub>/C<sub>2</sub> is one of the most abundant proteins in cells. In this manuscript, we showed that both hnRNP C<sub>1</sub> and C<sub>2</sub> promoted exon 11 inclusion of Ron pre-mRNA and that hnRNP C<sub>1</sub> and hnRNP C<sub>2</sub> functioned independently but not cooperatively. Moreover, hnRNP C<sub>1</sub> stimulated exon 11 splicing through intron 10 activation but not through intron 11 splicing. Furthermore, we showed that, whereas the RRM domain was required for hnRNP C<sub>1</sub> function, the Asp/Glu domain was not. In conclusion, hnRNP C<sub>1</sub>/C<sub>2</sub> promoted exon 11 splicing independently by stimulating intron 10 splicing through RRM but not through the Asp/Glu domain. [BMB Reports 2019; 52(11): 641-646]
SRSF2 directly inhibits intron splicing to suppresses cassette exon inclusion
( Heegyum Moon ),( Sunghee Cho ),( Tiing Jen Loh ),( Ha Na Jang ),( Yongchao Liu ),( Namjeong Choi ),( Jagyeong Oh ),( Jiyeon Ha ),( Jianhua Zhou ),( Sungchan Cho ),( Dong-eun Kim ),( Michael B. Ye ) 생화학분자생물학회(구 한국생화학분자생물학회) 2017 BMB Reports Vol.50 No.8
SRSF2, a Serine-Arginine rich (SR) protein, is a splicing activator that mediates exon inclusion and exclusion events equally well. Here we show SRSF2 directly suppresses intron splicing to suppress cassette exon inclusion in SMN pre-mRNA. Through a serial mutagenesis, we demonstrate that a 10 nt RNA sequence surrounding the branch-point (BP), is important for SRSF2-mediated inhibition of cassette exon inclusion through directly interacting with SRSF2. We conclude that SRSF2 inhibits intron splicing to promote exon exclusion. [BMB Reports 2017; 50(8): 423-428]