RNA polymerase II transcription on the fast lane

Marcello, Alessandro

doi:10.4161/trns.3.1.19147

Cited by 7 publications

(6 citation statements)

References 76 publications

(80 reference statements)

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“…In eukaryotes, genomeaverage DNA replication rates (the size of genome over the replication time ϫ the calculated number of replication forks), at 40 to 100 bp/s in yeast (105) and 10 to 60 bp/s in human cells (106), are similar to the mRNA transcription rates, at 30 to 60 nucleotides (nt)/s (107,108) (Fig. 2B), so there is no conflict between the two processes except maybe in the rRNA gene arrays, where the rate is regulated by the replication fork barriers (78) and is further reduced due to the extra replication origins.…”

Section: Functional Differencesmentioning

confidence: 94%

The Precarious Prokaryotic Chromosome

Kuzminov

2014

J Bacteriol

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Evolutionary selection for optimal genome preservation, replication, and expression should yield similar chromosome organizations in any type of cells. And yet, the chromosome organization is surprisingly different between eukaryotes and prokaryotes. The nuclear versus cytoplasmic accommodation of genetic material accounts for the distinct eukaryotic and prokaryotic modes of genome evolution, but it falls short of explaining the differences in the chromosome organization. I propose that the two distinct ways to organize chromosomes are driven by the differences between the global-consecutive chromosome cycle of eukaryotes and the local-concurrent chromosome cycle of prokaryotes. Specifically, progressive chromosome segregation in prokaryotes demands a single duplicon per chromosome, while other "precarious" features of the prokaryotic chromosomes can be viewed as compensations for this severe restriction.

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Section: Functional Differencesmentioning

confidence: 94%

The Precarious Prokaryotic Chromosome

Kuzminov

2014

J Bacteriol

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“…The rate of viral RNA biogenesis determines the amount of unspliced and partially spliced RNAs that are formed at the transcription site. In fact the high transcription rate observed for the HIV-1 provirus also resulted in the presence of a large fraction of unspliced RNAs at the transcription site possibly indicating an effect of RNAPII velocity on splicing efficiency as was recently proposed [33,34]. This RNA is either spliced or quickly degraded by the action of INS-binding factors and unknown nucleases.…”

Section: Discussionmentioning

confidence: 73%

“…These data were confirmed by the quantification of single (spliced) RNAs per cell at steady state reaching the conclusion that the output rate of HIV-1 transcription was of one new RNA every 1.2–2.4 seconds. These studies demonstrate that Tat-mediated HIV-1 transcription is highly efficient and able to produce a large amount of pre-mRNA in a short time [34]. But how is the downstream processing controlled in order to produce the large variety of RNA species characteristic of HIV-1?…”

Section: Spatial and Temporal Definition Of Hiv-1 Transcriptionmentioning

confidence: 99%

Dynamic Post-Transcriptional Regulation of HIV-1 Gene Expression

Kula

Marcello

2012

Biology

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Gene expression of the human immunodeficiency virus type 1 (HIV-1) is a highly regulated process. Basal transcription of the integrated provirus generates early transcripts that encode for the viral products Tat and Rev. Tat promotes the elongation of RNA polymerase while Rev mediates the nuclear export of viral RNAs that contain the Rev-responsive RNA element (RRE). These RNAs are exported from the nucleus to allow expression of Gag-Pol and Env proteins and for the production of full-length genomic RNAs. A balance exists between completely processed mRNAs and RRE-containing RNAs. Rev functions as an adaptor that recruits cellular factors to re-direct singly spliced and unspliced viral RNAs to nuclear export. The aim of this review is to address the dynamic regulation of this post-transcriptional pathway in light of recent findings that implicate several novel cellular cofactors of Rev function.

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“…Recent advances in live cell imaging allowed direct measurements of RNA biogenesis from the HIV-1 promoter exceeding 50 kb min -1 [298]. The studies of Marcello and collaborators demonstrate that Tat-mediated HIV-1 transcription is highly efficient and able to produce a large amount of pre-mRNA in a short time [299].…”

Section: Regulation Of Hiv-1 Gene Expression and Latency: Mechanisms mentioning

confidence: 99%

HIV-1 transcription and latency: an update

2013

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Combination antiretroviral therapy, despite being potent and life-prolonging, is not curative and does not eradicate HIV-1 infection since interruption of treatment inevitably results in a rapid rebound of viremia. Reactivation of latently infected cells harboring transcriptionally silent but replication-competent proviruses is a potential source of persistent residual viremia in cART-treated patients. Although multiple reservoirs may exist, the persistence of resting CD4+ T cells carrying a latent infection represents a major barrier to eradication. In this review, we will discuss the latest reports on the molecular mechanisms that may regulate HIV-1 latency at the transcriptional level, including transcriptional interference, the role of cellular factors, chromatin organization and epigenetic modifications, the viral Tat trans-activator and its cellular cofactors. Since latency mechanisms may also operate at the post-transcriptional level, we will consider inhibition of nuclear RNA export and inhibition of translation by microRNAs as potential barriers to HIV-1 gene expression. Finally, we will review the therapeutic approaches and clinical studies aimed at achieving either a sterilizing cure or a functional cure of HIV-1 infection, with a special emphasis on the most recent pharmacological strategies to reactivate the latent viruses and decrease the pool of viral reservoirs.

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RNA polymerase II transcription on the fast lane

Cited by 7 publications

References 76 publications

The Precarious Prokaryotic Chromosome

The Precarious Prokaryotic Chromosome

Dynamic Post-Transcriptional Regulation of HIV-1 Gene Expression

HIV-1 transcription and latency: an update

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