P1/HC-Pro of the Potyvirus targets RISC assembly (Brigneti et al., 1998; Anandalakshmi et al., 1998 ; Kasschau et al., 2003), 2b of Cucumber mosaic virus (CMV) binds to dsRNA and interferes with spread of silencing signal (Brigneti et al.,1998 ; Qi et al., 2004), p19 of tombusviruses binds to siRNAs (Voinnet et al., 1999; Silhavy et al., 2002 ; Qi et al., 2004), p38 encoded by the Turnip crinkle virus binds AGO1 and inhibits the activity of DCL-4 (Thomas et al., 2003; Azevedo et al., 2010), P25 of Potato Virus X interferes with the spread of silencing signal (Voinnet et al., 2000), P23, S, γb, P15, P0, P1, P30, P69, NS and coat protein of closterovirus (Reed et al., 2003 ; Lu et al., 2004), comovirus (Liu et al., 2004), hordeivirus …show more content…
Contrary to RNA viruses that can be controlled only by PTGS, geminiviruses may be manipulated by both PTGS and TGS. TGS is introduced when siRNAs corresponding to the promoter regions are produced that direct methylation of the promoter followed by inhibition of transcription (Mette et al., 2000). In a transient assay, TGS was reported to be effective against the begomovirus Mungbean yellow mosaic virus (Pooggin et al., 2003).
Viral invasiveness is reported to be promoted by the ability of C1 to suppress PTGS (Cui et al., 2005). It has been shown that C4 gene of Cotton leaf curl Multan virus and βC1gene of Cotton leaf curl Multan betasatellite bind short RNAs, with a preference for the double stranded and single stranded forms, respectively, suggesting that these suppressors sequester siRNAs and prevent their incorporation into the RNA-induced silencing complex (RISC) involved in sequence specific mRNA degradation (Hammond et al., 2000).
V2, a unique protein of monopartite begomoviruses has been shown to suppress PTGS in transient assays (Zrachya et al., 2007). It was demonstrated that ability of V2 to interact with SISG3, the tomato homologue of Arabidopsis SGS3 leads to suppression of PTGS (Glick et al., 2008). Furthermore, it was shown that the Rep proteins encoded by two alphasatellites, Gossypium darwinii symptomless alphasatellite and Gossypium mustelinium symptomless alphasatellite possess suppressor activity (Nawaz-ul-Rehman et
RNA interference, or RNAi, is a biological process in which RNA molecules reduce the gene expression of an organism. This is done typically by causing the destruction of specific mRNA molecules. RNAs are direct products of genes, these small RNAs can bind to other mRNA molecules to either increase or decrease their activity like in the example of preventing an mRNA from producing a protein. There are two types of RNA molecules that are central to RNAi, these molecules are, micro RNA (miRNA) and small interfering RNA (siRNA).
In the article, we learn the Cache Valley virus is spreading quickly through mosquitos. In this unit we learned that viruses with RNA in their nucleic acid reproduce a lot faster than viruses that have DNA in their nucleic acid, therefore the Cache Valley virus probably has RNA in its nucleic acid. Throughout the unit we learned viruses can spread through many types of mediums such
On encountering a host cell, the retrovirus attaches itself to receptors on the surface of the host cell’s membrane. Once inside the cell, the capsid opens, releasing RNA and reverse transcriptase into the cell’s cytoplasm.
RSV is caused by TLR3 activation. It initiates infections by binding to a cellular receptor and then the viral envelope fuses with the plasma membrane. The virus attaches the cell through the main protein, the G protein and fuses with the plasma membrane of the host cell through the F protein. After penetration, the nucleocapsid of the virus is released into the cytoplasm where replication occurs (3). The viral RNA is like a template for mRNA (3). The mRNA’s job is to translate the viral proteins and complementary RNA serves as a template for virion RNA
Step 1: How will you identify the “vital” cellular protein that the virus targets for degradation? (Hint: think proteomics). (3 pts.)
The devastation of soil, natural habitat and the destruction of mass farmlands all caused by the notorious feral hogs that has become nature’s neighbor that we have all come to despise. Today I would like to discuss how this resilient species has impacted the natural environments, and how their population is soaring in numbers; and last I would like to propose solutions to address the current issues were are facing and how to manage them.
RSV belongs to the paramyxovirus family of viruses. The virion encompasses a helical nucleocapsid packaged in a lipoprotein envelope attained from the host cell plasma membrane during budding. The external surface of the envelope contains a periphery of surface spikes.
* Flaviviruses: share a common size (40-60nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single stranded RNA approximately 10,000-11,000 bases), and appearance in the electron microscope. Therefore, images of West Nile virus are representative for this group of viruses.
Viruses are microscopic particles that invade and take over both eukaryotic and prokaryotic cells. They consist of two structures, which are the nucleic acid and capsid. The nucleic acid contains all genetic material in the form of DNA or RNA, and is enclosed in the capsid, which is the protein coating that helps the virus attach to and penetrate the host cell. In some cases, certain viruses have a membrane surrounding the capsid, called an envelope. This structure allows viruses to become more stealthy and protected. There are two cycles in which a virus can go into: lytic and lysogenic. The lytic cycle consists of the virus attaching to a cell, injecting its DNA, and creating more viruses, which proceed to destroy the host. On the other hand, the lysogenic cycle includes the virus attaching to the cell, injecting its DNA, which combines with the cell’s DNA in order for it to become provirus. Then, the provirus DNA may eventually switch to the lytic cycle and destroy the host.
The protective capsid helps the virus escape detection and destruction during the invasion of the host. When the virus reaches the target cell, biochemical reactions between the capsid and cell wall allow the virus to latch on and inject its genome into the cell’s interior. Once inside, the viral genetic material insinuates itself into the host’s DNA or RNA. In an efficient feat of natural bioengineering, the host cell’s genetic machinery now does the rest of the work for the virus. The cell, which had already been making copies of its own genome, now also replicates that of the virus. Coded within the viral material is the blueprint for making more copies of the viral genome. Further instructions command the production of capsids and directions for assembly of new viruses. After the host cell becomes engorged with viruses, it explodes, sending the new
The article first addresses the issue of whether or not to consider viruses as living. Although viruses used to be thought of as being biological chemicals due to the fact that they consist of nucleic acids
The similarity between the poliovirus and already solved plant virus’s led to a better understanding of how the poliovirus can regenerate within a host. Although the virus was similar to other plant viruses. The poliovirus was covered with more elaborate loops that are the site of monoclonal antibody escape mutations (Hogle, Chow and 229: 1358-1365Filman, Science). Individual proteins of the virus particle are produced by proteolytic cleavages from a larger precursor, yet the amino and carboxy-termini produced by proteolysis are very distinct. By noting this, Hogle and his team were able to conclude that proteolysis was not just making a lot of proteins from one gene, it is also controlling the timing of assembly (Hogle, Chow and Filman, Science 229: 1358-1365).
The HIV-1 virion is approximately 120 nm in diameter, roughly spherical, and is composed of two copies of a single stranded positive sense RNA enclosed by a capsid (24). The HIV-1 genome is less than 10 kb and encodes for more than nine different gene products. It encodes for 3 major structural protein genes: gag (group-specific antigen), pol (DNA polymerase), and env (Envelope), which code for major structural proteins and essential enzymes. Gag generates the mature Gag protein matrix (MA or p17), capsid (CA or p24), nucleocapsid (NC or p7), and p6, which encompass proteins for the basic infrastructure of the virus such as the inner core of the viral particle (25). Pol encodes for reverse transcriptase (RT), which enables the virus to reproduce, integrase (IN), which is necessary to integrate the viral double stranded DNA into the host genome, RNAse H, and HIV protease, which are all encapsulated in the core of the inner particle formed by the viral capsid protein p24 (25). Env encodes for glycoproteins of the outer membrane such as outer gp120 (which enables the virus to attach and fuse to cells of the host), and transmembrane gp41 that anchors the glycoprotein complex to the surface of the virion (25). Between the core and the envelope is the HIV matrix proteins which are composed of the viral protein p17 (23). HIV-1 also encodes for proteins with important regulatory elements (tat (Trans-Activator of Transcription) and rev
The virus responsible for rhizomania, beet necrotic yellow vein virus (BNYVV) is vectored by an
The microRNAs (miRNAs) are single-stranded small, endogenous, non-coding regulatory RNA with size varying ~21 to 24 nucleotides. microRNA mediated gene regulation play an important role in the negative regulation of gene at post-transcriptional level by targeting the mRNAs of protein coding genes by cleavage or repressing protein translation in eukaryotes and viruses (Bartel, 2004). microRNAs are expressed from their own genes located in the intergenic or intragenic region on the chromosomes (Lagos-Quintana et al., 2001). In plants, most miRNA genes are intergenic and transcribed individually from their own region, but a few genes are organized into polycistronic transcription units and co-transcribed from single promoter at the end of a