HnRNP G prevents inclusion on the HPV16 L1 mRNAs of the central exon between splice sites SA3358 and SD3632
(2018) In Journal of General Virology 99(3). p.328-343- Abstract
HPV16 late L1 mRNAs encode a short central exon that is located between HPV16 3′-splice site SA3358 and HPV16 5′-splice site SD3632. While SA3358 is used to produce both HPV16 early mRNAs encoding the E6 and E7 oncogenes, and late mRNAs encoding E4, L1 and L2, SD3632 is used exclusively to produce late L1 mRNA. We have previously identified an 8-nucleotide regulatory RNA element that is required for inclusion of the exon between SA3358 and SD3632 to produce L1 mRNAs at the expense of mRNAs polyadenylated at the HPV16 early polyadenylation signal pAE. Here we show that this HPV16 8-nucleotide splicing enhancer interacts with hnRNP G. Binding of hnRNP G to this element prevents inclusion of the exon between SA3358 and SD3632 on the HPV16... (More)
HPV16 late L1 mRNAs encode a short central exon that is located between HPV16 3′-splice site SA3358 and HPV16 5′-splice site SD3632. While SA3358 is used to produce both HPV16 early mRNAs encoding the E6 and E7 oncogenes, and late mRNAs encoding E4, L1 and L2, SD3632 is used exclusively to produce late L1 mRNA. We have previously identified an 8-nucleotide regulatory RNA element that is required for inclusion of the exon between SA3358 and SD3632 to produce L1 mRNAs at the expense of mRNAs polyadenylated at the HPV16 early polyadenylation signal pAE. Here we show that this HPV16 8-nucleotide splicing enhancer interacts with hnRNP G. Binding of hnRNP G to this element prevents inclusion of the exon between SA3358 and SD3632 on the HPV16 late L1 mRNAs. We concluded that hnRNP G has a splicing inhibitory role and that hnRNP G can control HPV16 mRNA splicing.
(Less)
- author
- Yu, Haoran LU ; Gong, Lijing LU ; Wu, Chengjun LU ; Nilsson, Kersti LU ; Li-Wang, Xiaoze LU and Schwartz, Stefan LU
- organization
- publishing date
- 2018-03-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- HnRNP G, Papillomavirus, Polyadenylation, Splicing, SR proteins
- in
- Journal of General Virology
- volume
- 99
- issue
- 3
- article number
- 001019
- pages
- 16 pages
- publisher
- Microbiology Society
- external identifiers
-
- pmid:29458523
- scopus:85043762470
- ISSN
- 0022-1317
- DOI
- 10.1099/jgv.0.001019
- language
- English
- LU publication?
- yes
- id
- 47dfd6b6-5b4a-41f2-ae5f-011fab693000
- date added to LUP
- 2018-03-27 13:54:56
- date last changed
- 2024-07-08 11:39:29
@article{47dfd6b6-5b4a-41f2-ae5f-011fab693000, abstract = {{<p>HPV16 late L1 mRNAs encode a short central exon that is located between HPV16 3′-splice site SA3358 and HPV16 5′-splice site SD3632. While SA3358 is used to produce both HPV16 early mRNAs encoding the E6 and E7 oncogenes, and late mRNAs encoding E4, L1 and L2, SD3632 is used exclusively to produce late L1 mRNA. We have previously identified an 8-nucleotide regulatory RNA element that is required for inclusion of the exon between SA3358 and SD3632 to produce L1 mRNAs at the expense of mRNAs polyadenylated at the HPV16 early polyadenylation signal pAE. Here we show that this HPV16 8-nucleotide splicing enhancer interacts with hnRNP G. Binding of hnRNP G to this element prevents inclusion of the exon between SA3358 and SD3632 on the HPV16 late L1 mRNAs. We concluded that hnRNP G has a splicing inhibitory role and that hnRNP G can control HPV16 mRNA splicing.</p>}}, author = {{Yu, Haoran and Gong, Lijing and Wu, Chengjun and Nilsson, Kersti and Li-Wang, Xiaoze and Schwartz, Stefan}}, issn = {{0022-1317}}, keywords = {{HnRNP G; Papillomavirus; Polyadenylation; Splicing; SR proteins}}, language = {{eng}}, month = {{03}}, number = {{3}}, pages = {{328--343}}, publisher = {{Microbiology Society}}, series = {{Journal of General Virology}}, title = {{HnRNP G prevents inclusion on the HPV16 L1 mRNAs of the central exon between splice sites SA3358 and SD3632}}, url = {{http://dx.doi.org/10.1099/jgv.0.001019}}, doi = {{10.1099/jgv.0.001019}}, volume = {{99}}, year = {{2018}}, }