2014
DOI: 10.1074/jbc.m113.521807
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Excision of Uracil from Transcribed DNA Negatively Affects Gene Expression

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Cited by 17 publications
(19 citation statements)
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“…These findings include (i) our previous report that multiple uracils silenced transcription from both HIV-1 LTR and CMV promoters in a cell line ( Weil et al, 2013 ), (ii) uracils within the origin of replication in HSV-1 perturb the binding of HSV-1 origin binding protein ( Focher et al, 1992 ), (iii) U/A pairs disrupt AP-1 transcription factor DNA binding ( Rogstad et al, 2002 ), (iv) singly uracilated DNA disrupts RNase H splicing specificity during reverse transcription Klarmann, 2003 , (v) U/A pairs perturb maintenance of telomere length in B cells by disruption of sheltrin binding ( Vallabhaneni et al, 2015 ), and (vi) one or two U/A base pairs within the specific cleavage site of some restriction enzymes prevents DNA strand cleavage ( Roberts et al, 2015 ). In addition, the abasic site product of uracil excision is known to exert a large negative effect on transcription ( Luhnsdorf et al, 2014 ) as would any mutations in transcription factor recognition sequences arising from error prone repair of excised uracils ( Shah et al, 2015 ; Emiliani, 1998 ). Combined, these potential effects of U/A pairs could profoundly silence HIV gene expression.…”
Section: Discussionmentioning
confidence: 99%
“…These findings include (i) our previous report that multiple uracils silenced transcription from both HIV-1 LTR and CMV promoters in a cell line ( Weil et al, 2013 ), (ii) uracils within the origin of replication in HSV-1 perturb the binding of HSV-1 origin binding protein ( Focher et al, 1992 ), (iii) U/A pairs disrupt AP-1 transcription factor DNA binding ( Rogstad et al, 2002 ), (iv) singly uracilated DNA disrupts RNase H splicing specificity during reverse transcription Klarmann, 2003 , (v) U/A pairs perturb maintenance of telomere length in B cells by disruption of sheltrin binding ( Vallabhaneni et al, 2015 ), and (vi) one or two U/A base pairs within the specific cleavage site of some restriction enzymes prevents DNA strand cleavage ( Roberts et al, 2015 ). In addition, the abasic site product of uracil excision is known to exert a large negative effect on transcription ( Luhnsdorf et al, 2014 ) as would any mutations in transcription factor recognition sequences arising from error prone repair of excised uracils ( Shah et al, 2015 ; Emiliani, 1998 ). Combined, these potential effects of U/A pairs could profoundly silence HIV gene expression.…”
Section: Discussionmentioning
confidence: 99%
“…Isogenic HeLa-derived cell lines in which TDG, SMUG1 or UNG1/2 DNA glycosylases were knocked down by stable expression of the specific shRNA and the corresponding control HeLa/pEpS cell line were generated and characterised by western blotting and the specific DNA glycosylase activity testing previously ( 29 ). The sequence cloned into the pENTR/pSuper+ vector (Addgene, Cambridge, MA, USA) for expression of shRNA which efficiently targets human TDG was 5′ GATCCGGGAACGAAATATGGACGTTCAACTCGAGTTGAACGTCCATATTTCGTTCTTTTTGGAAA.…”
Section: Methodsmentioning
confidence: 99%
“…To overcome this hurdle, we have previously proposed an efficient procedure for a site-specific incorporation of synthetic oligonucleotides containing various base modifications into plasmid-borne reporter genes with the help of sequence-specific nicking endonucleases ( 26 ). With these tools, we have already obtained important insights into the mechanisms of excision repair of several types of structurally defined DNA lesions in functional reporter genes ( 27 29 ). Here, we applied an analogous approach to measure the functional impacts of 5-mC, 5-hmC, 5-fC and 5-caC on the regulation of gene transcription.…”
Section: Introductionmentioning
confidence: 99%
“…In contrast to 3meA, AP site intermediates, generated by APE1 during BER, impair RNA pol II progression 43 . Finding that AAG, similarly to other DNA glycosylases 37 , primarily inhibits gene expression ( Fig. 1g) suggests that by coordinating BER initiation with transcription, AAG could potentially inhibit RNA pol II progression and therefore repress generation of faulty transcripts.…”
Section: Discussionmentioning
confidence: 99%
“…It has been suggested that for efficient repair within chromatin to take place, BER needs to be associated with essential nuclear processes, such as transcription 6 . Besides the potential importance of transcription in promoting efficient BER, several studies indicated that BER enzymes, in particular DNA glycosylases, could influence transcription and play an important role in modulation of gene expression [18][19][20]37 . However, direct evidence for the existence of transcription associated BER has not been provided so far.…”
Section: Discussionmentioning
confidence: 99%