@article{mbs:/content/journal/jgv/10.1099/vir.0.033183-0, author = "Somberg, Monika and Li, Xiaoze and Johansson, Cecilia and Orru, Beatrice and Chang, Roger and Rush, Margaret and Fay, Joanna and Ryan, Fergus and Schwartz, Stefan", title = "Serine/arginine-rich protein 30c activates human papillomavirus type 16 L1 mRNA expression via a bimodal mechanism", journal= "Journal of General Virology", year = "2011", volume = "92", number = "10", pages = "2411-2421", doi = "https://doi.org/10.1099/vir.0.033183-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.033183-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "Two splice sites on the human papillomavirus type 16 (HPV-16) genome are used exclusively by the late capsid protein L1 mRNAs: SD3632 and SA5639. These splice sites are suppressed in mitotic cells. This study showed that serine/arginine-rich protein 30c (SRp30c), also named SFRS9, activated both SD3632 and SA5639 and induced production of L1 mRNA. Activation of HPV-16 L1 mRNA splicing by SRp30c required an intact arginine/serine-repeat (RS) domain of SRp30c. In addition to this effect, SRp30c could enhance L1 mRNA production indirectly by inhibiting the early 3′-splice site SA3358, which competed with the late 3′-splice site SA5639. SRp30c bound directly to sequences downstream of SA3358, suggesting that SRp30c inhibited the enhancer at SA3358 and caused a redirection of splicing to the late 3′-splice site SA5639. This inhibitory effect of SRp30c was independent of its RS domain. These results suggest that SRp30c can activate HPV-16 L1 mRNA expression via a bimodal mechanism: directly by stimulating splicing to late splice sites and indirectly by inhibiting competing early splice sites.", }