Serine/arginine-rich protein 30c activates human papillomavirus type 16 L1 mRNA expression via a bimodal mechanism

Summary, in English

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.

• Författare: Monika Somberg; Xiaoze Li; Cecilia Johansson; Beatrice Orru; Roger Chang; Margaret Rush; Joanna Fay; Fergus Ryan; Stefan Schwartz
• Avdelning/ar: Avdelningen för medicinsk mikrobiologi
• Publiceringsår: 2011
• Språk: Engelska
• Sidor: 2411-2421
• Publikation/Tidskrift/Serie: Journal of General Virology
• Volym: 92
• Länkar: http://dx.doi.org/10.1099/vir.0.033183-0
• Dokumenttyp: Artikel i tidskrift
• Förlag: Microbiology Society
• Ämne: Microbiology in the medical area
• Status: Published
• ISBN/ISSN/Övrigt: ISSN: 1465-2099