scholarly journals SARS-CoV-2 Transgressing LncRNAs Uncovers the Known Unknowns

2021 ◽  
Author(s):  
Nidhi Shukla ◽  
Anchita Prasad ◽  
Uma Kanga ◽  
Renuka Suravajhala ◽  
Vinod Kumar Nigam ◽  
...  
Keyword(s):  
Viral Infection ◽  
Noncoding Rnas ◽  
Viral Proteins ◽  
Viral Pathogenesis ◽  
Long Noncoding Rnas ◽  
Open Reading Frames ◽  
Regulatory Role ◽  
Disease Pathogenesis ◽  
Known Unknowns ◽  
Reading Frames

SARS-CoV-2 harbors many known unknown regions in the form of hypothetical open reading frames (ORFs). While the mechanisms underlying the disease pathogenesis are not clearly understood, molecules such as long noncoding RNAs (lncRNAs) play a key regulatory role in the viral pathogenesis from endocytosis. We asked whether or not the lncRNAs in the host are associated with the viral proteins and argue that lncRNA-mRNA molecules related to viral infection may regulate SARS-CoV-2 pathogenesis. Towards the end of the perspective, we provide challenges and insights into investigating these transgression pathways.

scholarly journals When Long Noncoding Becomes Protein Coding

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Corrine Corrina R. Hartford ◽  
Ashish Lal
Keyword(s):  
Cell Division ◽  
Cell Signaling ◽  
Transcription Regulation ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Open Reading Frames ◽  
Protein Coding ◽  
Small Proteins ◽  
Coding Potential ◽  
Reading Frames

ABSTRACT Recent advancements in genetic and proteomic technologies have revealed that more of the genome encodes proteins than originally thought possible. Specifically, some putative long noncoding RNAs (lncRNAs) have been misannotated as noncoding. Numerous lncRNAs have been found to contain short open reading frames (sORFs) which have been overlooked because of their small size. Many of these sORFs encode small proteins or micropeptides with fundamental biological importance. These micropeptides can aid in diverse processes, including cell division, transcription regulation, and cell signaling. Here we discuss strategies for establishing the coding potential of putative lncRNAs and describe various functions of known micropeptides.

scholarly journals Widespread localisation of long noncoding RNAs to ribosomes: Distinguishing features and evidence for regulatory roles.

2015 ◽  
Author(s):  
Juna Carlevaro-Fita ◽  
Anisa Rahim ◽  
Roderic Guigo ◽  
Leah Vardy ◽  
Rory Johnson
Keyword(s):  
Transcriptional Regulation ◽  
Noncoding Rnas ◽  
Cell Types ◽  
Long Noncoding Rnas ◽  
Open Reading Frames ◽  
Translation Machinery ◽  
Evolutionary Selection ◽  
Regulatory Interactions ◽  
Distinguishing Features ◽  
Reading Frames

The function of long noncoding RNAs (lncRNAs) depends on their location within the cell. While most studies to date have concentrated on their nuclear roles in transcriptional regulation, evidence is mounting that lncRNA also have cytoplasmic roles. Here we comprehensively map the cytoplasmic and ribosomal lncRNA population in a human cell. Three-quarters (74%) of lncRNAs are detected in the cytoplasm, the majority of which (62%) preferentially cofractionate with polyribosomes. Ribosomal lncRNA are highly expressed across tissues, under purifying evolutionary selection, and have cytoplasmic-to-nuclear ratios comparable to mRNAs and consistent across cell types. LncRNAs may be classified into three groups by their ribosomal interaction: non-ribosomal cytoplasmic lncRNAs, and those associated with either heavy or light polysomes. A number of mRNA-like features destin lncRNA for light polysomes, including capping and 5′UTR length, but not cryptic open reading frames or polyadenylation. Surprisingly, exonic retroviral sequences antagonise recruitment. In contrast, it appears that lncRNAs are recruited to heavy polysomes through basepairing to mRNAs. Finally, we show that the translation machinery actively degrades lncRNA. We propose that light polysomal lncRNAs are translationally engaged, while heavy polysomal lncRNAs are recruited indirectly. These findings point to extensive and reciprocal regulatory interactions between lncRNA and the translation machinery.

The regulatory role of long noncoding RNAs in cancer

2017 ◽  
Vol 391 ◽  
pp. 12-19 ◽  
Author(s):  
Ying Tang ◽  
Belamy B. Cheung ◽  
Bernard Atmadibrata ◽  
Glenn M. Marshall ◽  
Marcel E. Dinger ◽  
...  
Keyword(s):  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Regulatory Role

scholarly journals First Report of a Mesonivirus and Its Derived Small RNAs in an Aphid Species Aphis citricidus (Hemiptera: Aphididae), Implying Viral Infection Activity

2020 ◽  
Vol 20 (2) ◽  
Author(s):  
Tengyu Chang ◽  
Mengmeng Guo ◽  
Wei Zhang ◽  
Jinzhi Niu ◽  
Jin-Jun Wang
Keyword(s):  
Viral Infection ◽  
Small Rnas ◽  
Rna Virus ◽  
Aphid Species ◽  
Open Reading Frames ◽  
First Report ◽  
The Family ◽  
Interfering Rna ◽  
Unassigned Genus ◽  
Reading Frames

Abstract We report a new positive-sense single-stranded RNA (ss RNA+) virus from the brown citrus aphid Aphis citricidus. The 20,300 nucleotide (nt)-long viral genome contains five open-reading frames and encodes six conserved domains (TM2, 3CLpro, TM3, RdRp, Zm, and HEL1). Phylogenetic analysis and amino acid sequence analysis revealed this virus might belong to an unassigned genus in the family Mesoniviridae. The presence of the virus was also confirmed in the field population. Importantly, analysis of the virus-derived small RNAs showed a 22-nt peak, implying that viral infection triggers the small interfering RNA pathway as antiviral immunity in aphids. This is the first report of a mesonivirus in invertebrates other than mosquitoes.

scholarly journals Peptide-Induced Amyloid-Like Conformational Transitions in Proteins

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Vladimir Egorov ◽  
Natalia Grudinina ◽  
Andrey Vasin ◽  
Dmitry Lebedev
Keyword(s):  
Protein Conformation ◽  
Conformational Transitions ◽  
Structural Features ◽  
Open Reading Frames ◽  
Short Peptides ◽  
Disease Pathogenesis ◽  
Conformational Diseases ◽  
Physiological Processes ◽  
And Function ◽  
Reading Frames

Changes in protein conformation can occur both as part of normal protein functioning and during disease pathogenesis. The most common conformational diseases are amyloidoses. Sometimes the development of a number of diseases which are not traditionally related to amyloidoses is associated with amyloid-like conformational transitions of proteins. Also, amyloid-like aggregates take part in normal physiological processes such as memorization and cell signaling. Several primary structural features of a protein are involved in conformational transitions. Also the protein proteolytic fragments can cause the conformational transitions in the protein. Short peptides which could be produced during the protein life cycle or which are encoded by short open reading frames can affect the protein conformation and function.

scholarly journals Overexpression of 7a, a Protein Specifically Encoded by the Severe Acute Respiratory Syndrome Coronavirus, Induces Apoptosis via a Caspase-Dependent Pathway

2004 ◽  
Vol 78 (24) ◽  
pp. 14043-14047 ◽  
Author(s):  
Yee-Joo Tan ◽  
Burtram C. Fielding ◽  
Phuay-Yee Goh ◽  
Shuo Shen ◽  
Timothy H. P. Tan ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Cell Lines ◽  
Cellular Localization ◽  
Viral Proteins ◽  
Open Reading Frames ◽  
Structural Proteins ◽  
Dependent Pathway ◽  
Reading Frames ◽  
Viral Structural Proteins

ABSTRACT Besides genes that are homologous to proteins found in other coronaviruses, the severe acute respiratory syndrome coronavirus genome also contains nine other potential open reading frames. Previously, we have characterized the expression and cellular localization of two of these “accessory” viral proteins, 3a (previously termed U274) and 7a (previously termed U122). In this study, we further examined whether they can induce apoptosis, which has been observed clinically. We showed that the overexpression of 7a, but not of 3a or the viral structural proteins, nucleocapsid, membrane, and envelope, induces apoptosis. 7a induces apoptosis via a caspase-dependent pathway and in cell lines derived from different organs, including lung, kidney, and liver.

scholarly journals A Novel P/V/C Gene in a New Member of theParamyxoviridae Family, Which Causes Lethal Infection in Humans, Horses, and Other Animals

1998 ◽  
Vol 72 (2) ◽  
pp. 1482-1490 ◽  
Author(s):  
Lin-Fa Wang ◽  
Wojtek P. Michalski ◽  
Meng Yu ◽  
L. Ian Pritchard ◽  
Gary Crameri ◽  
...  
Keyword(s):  
Basic Protein ◽  
Viral Proteins ◽  
Open Reading Frames ◽  
Sequence Comparisons ◽  
V Protein ◽  
Reading Frame ◽  
Lethal Infection ◽  
The Family ◽  
Low Levels ◽  
Reading Frames

ABSTRACT In 1994, a new member of the family Paramyxoviridaeisolated from fatal cases of respiratory disease in horses and humans was shown to be distantly related to morbilliviruses and provisionally called equine morbillivirus (K. Murray et al., Science 268:94–97, 1995). To facilitate characterization and classification, the virus was purified, viral proteins were identified, and the P/V/C gene was cloned and sequenced. The coding strategy of the gene is similar to that of Sendai and measles viruses, members of the Paramyxovirusand Morbillivirus genera, respectively, in the subfamilyParamyxovirinae. The P/V/C gene contains four open reading frames, three of which, P, C, and V, have Paramyxovirinaecounterparts. The P and C proteins are larger and smaller, respectively, than are cognate proteins in members of the subfamily, and the V protein is made as a result of a single G insertion during transcription. The P/V/C gene has two unique features. (i) A fourth open reading frame is located between those of the C and V proteins and potentially encodes a small basic protein similar to those found in some members of the Rhabdoviridae andFiloviridae families. (ii) There is also a long untranslated 3′ sequence, a feature common in Filoviridaemembers. Sequence comparisons confirm that although the virus is a member of the Paramyxovirinae subfamily, it displays only low levels of homology with paramyxoviruses and morbilliviruses and negligible homologies with rubulaviruses.

scholarly journals NF-κB Signaling Regulates Expression of Epstein-Barr Virus BART MicroRNAs and Long Noncoding RNAs in Nasopharyngeal Carcinoma

2016 ◽  
Vol 90 (14) ◽  
pp. 6475-6488 ◽  
Author(s):  
Rob J. A. Verhoeven ◽  
Shuang Tong ◽  
Gaohong Zhang ◽  
Jingfeng Zong ◽  
Yixin Chen ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epstein Barr Virus ◽  
Noncoding Rnas ◽  
Viral Proteins ◽  
Long Noncoding Rnas ◽  
Barr Virus ◽  
Iκb Kinase ◽  
Lmp1 Expression ◽  
Epstein Barr ◽  
Bart Mirnas

ABSTRACTEpstein-Barr virus (EBV) expresses few viral proteins in nasopharyngeal carcinoma (NPC) but high levels of BamHI-A rightward transcripts (BARTs), which include long noncoding RNAs (lncRNAs) and BART microRNAs (miRNAs). It is hypothesized that the mechanism for regulation of BARTs may relate to EBV pathogenesis in NPC. We showed that nuclear factor-κB (NF-κB) activates the BART promoters and modulates the expression of BARTs in EBV-infected NPC cells but that introduction of mutations into the putative NF-κB binding sites abolished activation of BART promoters by NF-κB. Binding of p50 subunits to NF-κB sites in the BART promoters was confirmed in electrophoretic mobility shift assays (EMSA) and further demonstratedin vivousing chromatin immunoprecipitation (ChIP) analysis. Expression of BART miRNAs and lncRNAs correlated with NF-κB activity in EBV-infected epithelial cells, while treatment of EBV-harboring NPC C666-1 cells with aspirin (acetylsalicylic acid [ASA]) and the IκB kinase inhibitor PS-1145 inhibited NF-κB activity, resulting in downregulation of BART expression. Expression of EBV LMP1 activates BART promoters, whereas an LMP1 mutant which cannot induce NF-κB activation does not activate BART promoters, further supporting the idea that expression of BARTs is regulated by NF-κB signaling. Expression of LMP1 is tightly regulated in NPC cells, and this study confirmed that miR-BART5-5p downregulates LMP1 expression, suggesting a feedback loop between BART miRNA and LMP1-mediated NF-κB activation in the NPC setting. These findings provide new insights into the mechanism underlying the deregulation of BARTs in NPC and identify a regulatory loop through which BARTs support EBV latency in NPC.IMPORTANCENasopharyngeal carcinoma (NPC) cells are ubiquitously infected with Epstein-Barr virus (EBV). Notably, EBV expresses very few viral proteins in NPC cells, presumably to avoid triggering an immune response, but high levels of EBV BART miRNAs and lncRNAs which exhibit complex functions associated with EBV pathogenesis. The mechanism for regulation of BARTs is critical for understanding NPC oncogenesis. This study provides multiple lines of evidence to show that expression of BARTs is subject to regulation by NF-κB signaling. EBV LMP1 is a potent activator of NF-κB signaling, and we demonstrate that LMP1 can upregulate expression of BARTs through NF-κB signaling and that BART miRNAs are also able to downregulate LMP1 expression. It appears that aberrant NF-κB signaling and expression of BARTs form an autoregulatory loop for maintaining EBV latency in NPC cells. Further exploration of how targeting NF-κB signaling interrupts EBV latency in NPC cells may reveal new options for NPC treatment.

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