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Article: Pseudouridylation of 7SK snRNA promotes 7SK snRNP formation to suppress HIV-1 transcription and escape from latency

TitlePseudouridylation of 7SK snRNA promotes 7SK snRNP formation to suppress HIV-1 transcription and escape from latency
Authors
Keywords7SK snRNA
HIV-1 transcription
latency
P-TEFb
pseudouridylation
Issue Date2016
Citation
EMBO Reports, 2016, v. 17, n. 10, p. 1441-1451 How to Cite?
AbstractThe 7SK snRNA sequesters P-TEFb, a general transcription elongation factor and human co-factor for HIV-1 Tat protein, into the catalytically inactive 7SK snRNP. Little is known about how 7SK RNA is regulated to perform this function. Here, we show that most of 7SK is pseudouridylated at position U250 by the predominant cellular pseudouridine synthase machinery, the DKC1–box H/ACA RNP. Pseudouridylation is critical to stabilize 7SK snRNP, as its abolishment by either mutation at or around U250 or depletion of DKC1, the catalytic component of the box H/ACA RNP, disrupts 7SK snRNP and releases P-TEFb to form the super elongation complex (SEC) and the Brd4–P-TEFb complex. The SEC is then recruited by Tat to the HIV-1 promoter to stimulate viral transcription and escape from latency. Thus, although 7SK RNA levels remain mostly unchanged, its function is modulated by pseudouridylation, which in turn controls transcription of both HIV-1 and cellular genes.
Persistent Identifierhttp://hdl.handle.net/10722/323988
ISSN
2023 Impact Factor: 6.5
2023 SCImago Journal Rankings: 3.193
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhao, Yang-
dc.contributor.authorKarijolich, John-
dc.contributor.authorGlaunsinger, Britt-
dc.contributor.authorZhou, Qiang-
dc.date.accessioned2023-01-13T03:00:43Z-
dc.date.available2023-01-13T03:00:43Z-
dc.date.issued2016-
dc.identifier.citationEMBO Reports, 2016, v. 17, n. 10, p. 1441-1451-
dc.identifier.issn1469-221X-
dc.identifier.urihttp://hdl.handle.net/10722/323988-
dc.description.abstractThe 7SK snRNA sequesters P-TEFb, a general transcription elongation factor and human co-factor for HIV-1 Tat protein, into the catalytically inactive 7SK snRNP. Little is known about how 7SK RNA is regulated to perform this function. Here, we show that most of 7SK is pseudouridylated at position U250 by the predominant cellular pseudouridine synthase machinery, the DKC1–box H/ACA RNP. Pseudouridylation is critical to stabilize 7SK snRNP, as its abolishment by either mutation at or around U250 or depletion of DKC1, the catalytic component of the box H/ACA RNP, disrupts 7SK snRNP and releases P-TEFb to form the super elongation complex (SEC) and the Brd4–P-TEFb complex. The SEC is then recruited by Tat to the HIV-1 promoter to stimulate viral transcription and escape from latency. Thus, although 7SK RNA levels remain mostly unchanged, its function is modulated by pseudouridylation, which in turn controls transcription of both HIV-1 and cellular genes.-
dc.languageeng-
dc.relation.ispartofEMBO Reports-
dc.subject7SK snRNA-
dc.subjectHIV-1 transcription-
dc.subjectlatency-
dc.subjectP-TEFb-
dc.subjectpseudouridylation-
dc.titlePseudouridylation of 7SK snRNA promotes 7SK snRNP formation to suppress HIV-1 transcription and escape from latency-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.15252/embr.201642682-
dc.identifier.pmid27558685-
dc.identifier.scopuseid_2-s2.0-84989870458-
dc.identifier.volume17-
dc.identifier.issue10-
dc.identifier.spage1441-
dc.identifier.epage1451-
dc.identifier.eissn1469-3178-
dc.identifier.isiWOS:000385710000009-

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