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. 2014 Jul 3;42(13):8343–8355. doi: 10.1093/nar/gku561

Figure 9.

Figure 9.

Proposed model of action of INXS lncRNA. BCL-X pre-mRNA undergoes either a BCL-XL anti-apoptotic or BCL-XS pro-apoptotic alternative processing (4). We propose that the control of BCL-X pre-mRNA alternative splicing, between pathway [1] toward BCL-XL anti-apoptotic isoform and pathway [2] toward BCL-XS pro-apoptotic isoform, depends on INXS endogenous lncRNA. Apoptosis inducing agents, such as UV-C light exposure, serum starvation or anti-cancer drugs, lead to an increased expression of endogenous INXS. Sam68 increases the level of the pro-apoptotic BCL-XS isoform, while its absence leads to the accumulation of BCL-XL (12). We propose that the augmented levels of INXS would favor the positioning of Sam68 splicing-modulator and of possible additional splice factors (SF) of the splicing machinery near the distal donor 5′ splice site on the pre-mRNA (5′ss, dotted blue line) and favor the splicing predominantly through pathway 2, thus leading to BCL-XS protein synthesis and to apoptosis.