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. 2009 Jul 30;28(18):2733–2747. doi: 10.1038/emboj.2009.216

Figure 6.

Figure 6

CRTC recruitment to promoters is sufficient to augment splicing but not transcriptional activation. (A) Schematic representation of the S1X-R minigene reporter substrates that substitute the LTR for the wild-type β-globin promoter or a β-globin promoter-containing tandem GAL4–UAS binding sites. (B) HEK293T cells co-transfected with the indicated reporter construct together with GAL4–CRTC1 or GAL4–CREB expression plasmids. RT–PCR products were separated by PAGE and splice variants analysed to determine the effect of CRTC recruitment to the β-globin promoter on splicing. Ratio of spliced versus unspliced exons are graphically displayed (n=3 experiments; mean±s.e.m.; asterisk denotes P-value ⩽0.05). (C) qPCR analysis of reporter gene expression. Relative amounts of HIV-1 reporter transcripts obtained by each transfection were plotted as fold of total gene products expressed (unspliced+spliced) versus the amount expressed by the pβGlo-S1X-R or pβGlo-GaS-S1X-R constructs (n=3 experiments; mean±s.e.m.; asterisk denotes P-value ⩽0.05).