Interplay of mRNA capping and transcription machineries

Kachaev, Zaur M.; Лебедева, Л. А.; Kozlov, Eugene; Shidlovskii, Yulii V.

doi:10.1042/bsr20192825

Cited by 15 publications

(19 citation statements)

References 101 publications

(145 reference statements)

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“…The aromates engage the m 7 G in pii-pii cation- pi stacking interactions that stabilize the 5′-end of the nascent RNA prior to the release of the paused polymerase. That CBC-m 7 G-cap stimulates the subsequent formation of pre-initiation complexes at the promoter suggested synergy between the post-transcriptional RNPs and transcriptional initiation events back at the promoter [ 34 ].…”

Section: Hiv Precursor Rnas Enter Mutually Exclusive Rna-fate Pathway...mentioning

confidence: 99%

Anomalous HIV-1 RNA, How Cap-Methylation Segregates Viral Transcripts by Form and Function

Boris‐Lawrie

Singh

Osmer

et al. 2022

Viruses

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The acquisition of m7G-cap-binding proteins is now recognized as a major variable driving the form and function of host RNAs. This manuscript compares the 5′-cap-RNA binding proteins that engage HIV-1 precursor RNAs, host mRNAs, small nuclear (sn)- and small nucleolar (sno) RNAs and sort into disparate RNA-fate pathways. Before completion of the transcription cycle, the transcription start site of nascent class II RNAs is appended to a non-templated guanosine that is methylated (m7G-cap) and bound by hetero-dimeric CBP80-CBP20 cap binding complex (CBC). The CBC is a nexus for the co-transcriptional processing of precursor RNAs to mRNAs and the snRNA and snoRNA of spliceosomal and ribosomal ribonucleoproteins (RNPs). Just as sn/sno-RNAs experience hyper-methylation of m7G-cap to trimethylguanosine (TMG)-cap, so do select HIV RNAs and an emerging cohort of mRNAs. TMG-cap is blocked from Watson:Crick base pairing and disqualified from participating in secondary structure. The HIV TMG-cap has been shown to license select viral transcripts for specialized cap-dependent translation initiation without eIF4E that is dependent upon CBP80/NCBP3. The exceptional activity of HIV precursor RNAs secures their access to maturation pathways of sn/snoRNAs, canonical and non-canonical host mRNAs in proper stoichiometry to execute the retroviral replication cycle.

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Section: Hiv Precursor Rnas Enter Mutually Exclusive Rna-fate Pathway...mentioning

confidence: 99%

Anomalous HIV-1 RNA, How Cap-Methylation Segregates Viral Transcripts by Form and Function

Boris‐Lawrie

Singh

Osmer

et al. 2022

Viruses

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“…The sequence of steps is illustrated in Fig 2. The critical pathways utilized by SARS-CoV-2 include a) RNA Synthesis, b) proofreading of template, and c) capping. [68] The RNA machinery involves Nsp1-16 complex, [68,69] among which Nsp12 (RNA dependent RNA polymerase; RdRp) [70,71], Nsp13 (zinc-binding helicase; HEL) [72], Nsp14-16 complex (mRNA capping) [73], Nsp14 (RNA proofreading) [70,74], Nsp15 (uridylate-specific Top left shows the virus structure identifying protruding surface spike proteins (enlarged to show S1 and S2 segments with the Receptor Binding Domain (RBD)), the most abundant Membrane protein, the Envelope protein that forms a simple multimeric ion channel, and the Nucleocapsid protein with the bound positive sense single strand (ss) RNA. Below: Furin pre-cleaves spike proteins at the S1/S2 site and promotes subsequent TMPRSS2-dependent entry into host cells.…”

Section: Translation and Rna Replicationmentioning

confidence: 99%

“…The critical pathways utilized by SARS-CoV-2 include a) RNA Synthesis, b) proofreading of template, and c) capping. [ 68 ] The RNA machinery involves Nsp1-16 complex,[ 68 , 69 ] among which Nsp12 (RNA dependent RNA polymerase; RdRp)[ 70 , 71 ], Nsp13 (zinc-binding helicase; HEL)[ 72 ], Nsp14-16 complex (mRNA capping)[ 73 ], Nsp14 (RNA proofreading)[ 70 , 74 ], Nsp15 (uridylate-specific endoribonuclease activity (NendoU))[ 29 ], and Nsp7–Nsp10 (non-structural proteins) are critical for virus. [ 74 ] All the machinery system is present in host cell endoplasmic reticulum in complex with the transcription enzyme of SARS-CoV-2.…”

Section: Sars-cov-2 Entry and Initiationmentioning

confidence: 99%

Drugs targeting various stages of the SARS-CoV-2 life cycle: Exploring promising drugs for the treatment of Covid-19

Ramarao

Joshi

Jagadeesh³

2020

Cellular Signalling

129

107

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a positive-sense, single-stranded RNA virus that causes the potentially lethal Covid-19 respiratory tract infection. It does so by binding to host cell angiotensin converting enzyme 2 (ACE2) receptors, leading to endocytosis with the receptor, and subsequently using the host cell's machinery to replicate copies of itself and invade new cells. The extent of the spread of infection in the body is dependent on the pattern of ACE2 expression and overreaction of the immune system. Additionally, by inducing an imbalance in the renin-angiotensin-aldosterone system (RAAS) and the loss of ACE2 would favour the progression of inflammatory and thrombotic processes in the lungs. No drug or vaccine has yet been approved to treat human coronaviruses. Hundreds of clinical trials on existing approved drugs from different classes acting on a multitude of targets in the virus life cycle are ongoing to examine potential effectiveness for the prevention and treatment of the infection. This review summarizes the SARS-CoV-2 virus life cycle in the host cell and provides a biological and pathological point of view for repurposed and experimental drugs for this novel coronavirus. The viral life cycle provides potential targets for drug therapy.

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“…Enhancer transcription proceeds through the same steps as gene promoter transcripts, including TSS-proximal pausing, capping, and release [98,[106][107][108]. Early pausing was demonstrated for enhancer-like loci in human K562 cells and mouse embryonic fibroblasts (MEFs) [109].…”

Section: Pol II Pausing At Enhancersmentioning

confidence: 99%

Molecular Basis of the Function of Transcriptional Enhancers

Ibragimov

Bylino

Shidlovskii

2020

Cells

Self Cite

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Transcriptional enhancers are major genomic elements that control gene activity in eukaryotes. Recent studies provided deeper insight into the temporal and spatial organization of transcription in the nucleus, the role of non-coding RNAs in the process, and the epigenetic control of gene expression. Thus, multiple molecular details of enhancer functioning were revealed. Here, we describe the recent data and models of molecular organization of enhancer-driven transcription.

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Interplay of mRNA capping and transcription machineries

Cited by 15 publications

References 101 publications

Anomalous HIV-1 RNA, How Cap-Methylation Segregates Viral Transcripts by Form and Function

Anomalous HIV-1 RNA, How Cap-Methylation Segregates Viral Transcripts by Form and Function

Drugs targeting various stages of the SARS-CoV-2 life cycle: Exploring promising drugs for the treatment of Covid-19

Molecular Basis of the Function of Transcriptional Enhancers

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